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Air pollution is a rapidly growing major health concern around the world. Atmospheric particulate matter that has a diameter of less than 2.5 µm (PM2.5) refers to an air pollutant composed of particles and chemical compounds that originate from various sources. While epidemiological studies have established the association between PM2.5 exposure and cardiovascular diseases, the precise cellular and molecular mechanisms by which PM2.5 promotes cardiovascular complications are yet to be fully elucidated. In this review, we summarize the various sources of PM2.5, its components, and the concentrations of ambient PM2.5 in various settings. We discuss the experimental findings to date that evaluate the potential adverse effects of PM2.5 on cardiovascular homeostasis and function, and the possible therapeutic options that may alleviate PM2.5-driven cardiovascular damage.

Platelet derived growth factor B (PDGFB) / PDGFRβ signalling is a key regulator of the cardiovascular system in development, health, and disease. During angiogenesis PDGFB regulates pericyte migration and proliferation during development and in tissue repair. Pericytes confer vessel stability, maintain vessel integrity, and control vascular tone. In the field of regenerative medicine, pericytes have also risen to prominence as they were discovered to be the in-situ counterpart of mesenchymal stem/stromal cells (MSCs). Pdgfbret/ret mutantmice are pericyte-deficient. The PDGFB retention motif is deleted, reducing PDGFB retention in the pericellular space and extracellular matrix and therefore pericyte recruitment during angiogenesis. This reduction in vascular pericyte coverage in pdgfbret/ret mice manifests in phenotypic differences compared with pdgfb+/+ and pdgfbret/+ littermates. Of relevance, is the reported development of vascular associated brain calcification in 4–12-month-old pdgfbret/ret mice and alterations to left ventricular structure from 10 to 20 weeks of age. In this thesis, I have investigated the hypothesis that calcification develops throughout the vasculature in pdgfbret/ret mice and that alteration of left ventricular structure leads to a progressive decline in heart function. I also hypothesised that disruption to PDGFB/PDGFRβ signalling in vivo influences the in vitro properties of MSCs. To address my hypotheses, I used a combination of cardiovascular imaging techniques, positron emission tomography/computed tomography (PET/CT) and high-resolution cardiac ultrasound, alongside in vitro MSC osteogenic assays. Contrary to my original hypothesis, results of PET/CT imaging using 18F-NaF, a radioactive tracer with the propensity to bind to hydroxyapatite calcification, did not reveal any areas of ectopic calcification out with the brain in male or female pdgfbret/ret mice. No significant calcification was observed in the aortic arch, the descending thoracic aorta, heart, or kidneys. Indeed, calcification was restricted to the brain at 12 months of age and completely absent from pdgfb+/+ and pdgbret/+ littermates. However, I did observe that the extent and anatomical location of brain calcification was variable in pdgfbret/ret mice. Using high resolution cardiac ultrasound, I next evaluated the cardiac phenotype exhibited in male and female pdgfbret/ret mice over the course of 12 months. The results of this study reveal that both male and female pdgfbret/ret mice exhibit signs of cardiac dilation with increasing left ventricular end diastolic area at 3 months of age, whereas females exhibit an increase in left ventricular mass that may be the result of hypertrophic remodelling or oedema. However, over the course of 6, 9 and 12 months, this phenotype resolves in both male and female pdgfbret/ret mice and normal contractile function is maintained. Further analysis of cardiac structure and function was performed using speckle tracking echocardiography (STE) in a combined male and female cohort of pdgfb+/+, pdgfbret/+ and pdgfbret/ret mice. Using STE, subtle changes to segmental systolic and diastolic cardiac strain were detected at 9 and 12 months of age in pdgfbret/ret mice. These changes may preclude the onset of deterioration of cardiac function in pdgfbret/ret mice and requires further investigation beyond 12 months of age to conclude. Finally, I examined the effects of the pdgfbret mutation on the osteogenic potential of MSCs derived from large coronary vessels and various vascularised tissues including the kidney, the skeletal muscle, and the heart in vitro. Quantification of osteogenic potential saw an increase in calcium deposition in combined pdgfbret MSC tissues. Tissue specific osteogenic potential was highly variable although there was a trend towards an increased osteogenesis in pdgfbret mutant tissues. Together, data from my studies indicate that pdgfbret/ret mice exhibit a transient cardiac phenotype which is ameliorated and have variable levels of calcification exclusive to the brain at 12 months of age. This data also indicates that MSCs derived from pdgfbret mutants have greater osteogenic potential although the tissue specificity of this potential requires further investigation.

Heart failure is characterized by the heart losing its capacity to pump sufficient blood to match the body’s demand. It is caused by a variety of cardiovascular impairments. Among them, atherosclerosis is the most common one. Although, a variety of medicines selectively target this pathology, the death rate due to atherosclerosis associated heart disorders remain high. To address this issue, the use of antioxidants combined with conventional therapy to achieve synergistic effects has gained popularity. Melatonin is one of such antioxidants. In addition to its potent antioxidant activity, this molecule acts in harmony to protect the cardiovascular tissue. This review explores the various mechanisms by which melatonin protects the cardiovascular tissue. This information will contribute further insights into the role of melatonin in maintaining cardiovascular homeostasis in normal as well as in pathological conditions. It will also help us to better understand the potential synergistic effects of melatonin with conventional therapy to successfully target the heart failure associated with atherosclerosis.

Disorders of fluid balance and electrolyte homeostasis are commonly observed in critically ill patients and in those who require emergency anaesthesia. Consequently, anaesthetists and intensive care physicians must understand the physiological principles that govern fluid balance. This article discusses the compartmentalization of total body water and describes methods by which the volume of the fluid compartments may be measured. The novel concept of the endothelial glycocalyx is discussed in addition to the conventional and contemporary models of capillary filtration dynamics. The core elements of fluid balance and cardiovascular homeostasis are also explored.

Excessive consumption of fructose, the sweetest of all naturally occurring carbohydrates, has been linked to worldwide epidemics of metabolic diseases in humans, and it is considered an independent risk factor for cardiovascular diseases. We provide an overview about the features of fructose metabolism, as well as potential mechanisms by which excessive fructose intake is associated with the pathogenesis of metabolic diseases both in humans and rodents. To accomplish this aim, we focus on illuminating the cellular and molecular mechanisms of fructose metabolism as well as its signaling effects on metabolic and cardiovascular homeostasis in health and disease, highlighting the role of carbohydrate-responsive element–binding protein in regulating fructose metabolism.

The history of hydrogen sulphide (H 2 S), which is a toxic, colourless gas with peculiar, creepy smell of rotten eggs is long. It’s critical role not only in development of the Universe but also in evolution of living organisms has been well documented. Apart from the contribution in evolution the hydrogen sulphide has been recognized as an important gasotransmitter in numerous biological processes. In the paper we review recent discoveries on dominating pathways leading to synthesis of endogenous hydrogen sulphide, we summarize the key biological effects of hydrogen sulphide of importance for cardiovascular homeostasis. Further, we point out selected molecules of natural origin and also products of chemical synthesis known to increase via different mechanisms the bioavailability of hydrogen sulphide. Among drugs approved for human pharmacotherapy zofenopril is the one shown to possess such an ability. The drug belongs to angiotensin-converting enzyme inhibitors (ACEIs) having sulfhydryl moiety in its chemical structure. One of the metabolite of zofenopril was shown to increase the expression of enzyme synthesizing hydrogen sulphide and to elevate both plasma and myocardial levels of hydrogen sulphide. The above mentioned effects have not been shown by using other ACEI. Hydrogen sulphide realising ability of zofenopril apart of its long-term inhibition of ACEIs may be considered as potential explanation for prognostic advantage over other drugs of the same class shown in prospective randomised trial.

Severe acute respiratory syndrome coronavirus 2, which is responsible for the current coronavi-rus disease 2019 pandemic, uses angiotensin-converting enzyme 2 as a gateway into host cells In this review, we summarized the biology of this enzyme which plays a key role in cardiovascular homeostasis and blood pressure control Blockers of the renin-angiotensin-aldosterone system modify the expression and activity of angiotensin-converting enzyme 2, possibly in different ways The effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers on the expression and enzyme activity of angiotensin-converting enzyme 2 are reviewed, and the consequences of these treatments for the severity of coronavirus disease 2019 infection are discussed © 2020, John Libbey All rights reserved

The semipermeable capillary walls not only enable the removal of excess body water and solutes during hemodialysis (HD) but also provide an essential mechanism for maintaining cardiovascular homeostasis. Here, we investigated transcapillary transport processes on the whole-body level using the three-pore model of the capillary endothelium with large, small and ultrasmall pores. The transcapillary transport and cardiovascular response to a 4-h hemodialysis (HD) with 2 L ultrafiltration were analyzed by simulations in a virtual patient using the three-pore model of the capillary wall integrated in the whole-body compartmental model of the cardiovascular system with baroreflex mechanisms. The three-pore model revealed substantial changes during HD in the magnitude and direction of transcapillary water flows through small and ultrasmall pores and associated changes in the transcapillary convective transport of proteins and small solutes. The fraction of total capillary hydraulic conductivity attributed to ultrasmall pores was found to play an important role in the transcapillary water transport during HD thus influencing the cardiovascular response to HD. The presented model provides a novel computational framework for a detailed analysis of microvascular exchange during HD and as such may contribute to a better understanding of dialysis-induced changes in blood volume and blood pressure.

Blood pressure (BP) is one of the most dynamic physiologic variables that is routinely measured in clinical practice and is characterized by continuous and significant changes beat-to-beat, over 24 h, day-to-day, and visit-to-visit. Under physiological conditions, these BP variations largely represent a response to environmental stimulations and challenges of daily life aimed at maintaining so-called cardiovascular “homeostasis”. However, sustained increases in blood pressure variability (BPV) may also reflect alterations in cardiovascular regulatory mechanisms or underlying pathological conditions and may represent a source of damage to the cardiovascular system. The clinical significance and prognostic implications of these BP variations have been demonstrated by a series of clinical and population studies conducted in recent years, in which increasing BPV has been associated with a higher risk of subclinical organ damage, cardiovascular events, and cardiovascular and all-cause mortality, independent of elevated average BP values. This paper will review the available evidence on the current definitions, classification, and mechanisms responsible for different types of BPV by focusing on their relevance to cardiovascular homeostasis and cardiovascular disease.

Despite the long history of the concept where infection plays a significant role in cardiovascular diseases (atherosclerosis in particular), today it is relevant and represented a significant interest.This article discusses H. pylori role in mechanisms of cardiovascular homeostasis disturbance. H. pylori involvement in atherogenic damage of arteries, and/or plaque destabilization is no doubt. This vidence is detailed in this review article.

In quadrupeds, the arterial baroreflex has dominance in the reflex homeostatic responses, which protect against haemorrhage. In humans, it is the low pressure cardiopulmonary reflex, which protects against the analogous cardiovascular challenge of gravity-dependent venous pooling with standing. To preserve orthostatic cardiovascular homeostasis with the emergence of bipedalism in humans the low pressure reflex, a minor, subsidiary reflex in quadripeds, was co-opted. Mirroring the imperfect skeletal evolution to bipedalism, this cardiovascular development has been problematic, with dysregulation manifesting as disabling orthostatic intolerance syndromes and, paradoxically, an orthostatic hypertensive response that appears to play a role in the development of essential hypertension in some people. Improved understanding of these evolutionary faults provides new options for postural and pharmacological treatments.

Nitric oxide (NO) is a key molecule in cardiovascular homeostasis and its abnormal delivery is highly associated with the occurrence and development of cardiovascular disease (CVD). The assessment and manipulation of NO delivery is crucial to the diagnosis and therapy of CVD, such as endothelial dysfunction, atherosclerotic progression, pulmonary hypertension, and cardiovascular manifestations of coronavirus (COVID-19). However, due to the low concentration and fast reaction characteristics of NO in the cardiovascular system, clinical applications centered on NO delivery are challenging. In this tutorial review, we first summarized the methods to estimate the in vivo NO delivery process, based on computational modeling and flow-mediated dilation, to assess endothelial function and vulnerability of atherosclerotic plaque. Then, emerging bioimaging technologies that have the potential to experimentally measure arterial NO concentration were discussed, including Raman spectroscopy and electrochemical sensors. In addition to diagnostic methods, therapies aimed at controlling NO delivery to regulate CVD were reviewed, including the NO release platform to treat endothelial dysfunction and atherosclerosis and inhaled NO therapy to treat pulmonary hypertension and COVID-19. Two potential methods to improve the effectiveness of existing NO therapy were also discussed, including the combination of NO release platform and computational modeling, and stem cell therapy, which currently remains at the laboratory stage but has clinical potential for the treatment of CVD.

Great progress has been made in the understanding of the pathophysiology of cardiovascular diseases (CVDs), and this has improved the prevention and prognosis of CVDs. However, while sex differences in CVDs have been well documented and studied for decades, their full extent remains unclear. Results of the latest clinical studies provide strong evidence of sex differences in the efficacy of drug treatment for heart failure, thereby possibly providing new mechanistic insights into sex differences in CVDs. In this review, we discuss the significance of sex differences, as rediscovered by recent studies, in the pathogenesis of CVDs. First, we provide an overview of the results of clinical trials to date regarding sex differences and hormone replacement therapy. Then, we discuss the role of sex differences in the maintenance and disruption of cardiovascular tissue homeostasis.

MiRNA-regulated processes are pivotal in cardiovascular homeostasis and disease. These short non-coding RNAs have ideal properties that could be utilized as potential biomarkers; moreover, their functions as post-transcriptional regulators of mRNA make them interesting therapeutic targets. In this review, we summarize the current state of miRNA-based biomarkers in a variety of diseases leading to heart failure, as well as provide an outlook on developing miRNA-based therapies in the heart failure field.

Background: L-Arginine is an amino acid which is involved in nitric oxide production regulating vascular tone and cardiovascular homeostasis. Hypertension is one of the most common comorbidities worldwide, and leads to endothelial dysfunction contributing to atherosclerosis, inflammation, and oxidative stress. Frailty is a syndrome of decreased physiological reserves with increased susceptibility to stressors leading to higher mortality, hospitalization, disability, and functional and cognitive impairment. Cognitive impairment is a very common feature in hypertensive frail older adults. Hence, it is very important to treat cognitive impairment to delay and/or prevent adverse events. Our study, thus, investigated the effects of 4-weeks supplementation of L-Arginine on global cognitive function. Methods: We studied 101 frail older patients from April 2020 to April 2021. All subjects were recruited from ASL (local health company of Italian Ministry of Health) Avellino, Italy. All patients fulfilled all of the following inclusion criteria: a previous diagnosis of hypertension, a confirmed frail status, age >65 years. The exclusion criteria were: age Results: We are reporting here the results in 52 patients who hitherto successfully completed the study. The cognitive screening was available at baseline (before treatment) and during a follow-up of 4 weeks. The non-treated group (n=27) had a Montreal Cognitive Assessment (MoCA) score 22.9±0.9 at basal and 23.4±1.0 at follow-up (p=0.06). The treated group (oral L-Arginine, 1.66 g, twice a day; n=25) displayed a MoCA score 23.1±0.7 at basal and 24.2±0.6 at follow-up (p Conclusions: Our data show a significant improvement in the MoCA score in the group treated with L-Arginine. More extensive studies are needed to verify the efficacy of L-Arginine in this population.

The effects of the apelinergic system components apelin (AP) and elabela (ELA) in the regulation of human cardiovascular homeostasis, and data concerning the relationship between ELA and AP and coronary artery disease (CAD) are yet unknown. The aim of the study was the evaluation of AP, ELA and APJ-receptor levels in the plasma of patients with chronic coronary syndromes (CCS) and acute coronary syndromes (ACS). The study group consisted of 114 patients with CAD and 33 healthy controls. Patients were divided into two groups: with CCS (n = 30) and ACS (n = 84). Routine laboratory tests and plasma ELA, AP-17, AP-13 and APJ receptor levels were measured. Echocardiographic data were analyzed in all patients. Levels of AP-17 and ELA were significantly lower in CCS than in healthy controls and ACS patients. We demonstrated significant increase of levels of plasma apelinergic system peptides, especially ELA and AP-17 in ACS patients compared with healthy controls and CCS, suggestive of compensating up-regulation mechanisms. There is a relationship between circulating ELA and AP-17 levels and classical, biochemical markers of ischemia and left ventricular ejection faction as well.

Fluctuation analysis in intervals between heartbeats provides important indices related to autonomic modulation of heart rate variability (HRV). These indices are considered predictors of morbidity and mortality as they are frequently altered in patients with chronic degenerative diseases, especially in those with cardiovascular and metabolic diseases. Similarly, a reduction in HRV is common with aging. In all cases, cardiovascular fitness is often reduced to below the predicted values. In turn, increases in cardiovascular fitness through regular physical exercise, especially aerobic exercise, represent an important therapeutic tool capable of promoting positive adjustments in cardiac autonomic modulation. These adjustments are characterized by reduced sympathetic modulatory influence and/or increased vagal modulatory influence on the heart, increasing the HRV. Therefore, several methodological tools have been used to assess the degree of impairment of autonomic modulation and the therapeutic effects of physical exercise. In contrast, establishment of strict protocols in experimental design is a main challenge in establishing HRV analysis as a robust parameter for evaluating cardiovascular homeostasis. Thus, this review aimed to contribute to the understanding of autonomic modulation of HRV and its relationship with cardiovascular fitness, highlighting the advances made thus far, the applicability of analysis tools, and the confounding factors observed frequently.

Cannabis is widely used for both recreational and medicinal purposes on a global scale. There is accumulating interest in the use of cannabis and its constituents for athletic recovery, and in some instances, performance. Amidst speculation of potential beneficial applications, the effects of cannabis and its two most abundant constituents, delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD), remain largely un-investigated. The purpose of this review is to critically evaluate the literature describing the effects of whole cannabis, THC, and CBD, on athletic performance and recovery. While investigations of whole cannabis and THC have generally shown either null or detrimental effects on exercise performance in strength and aerobic-type activities, studies of sufficient rigor and validity to conclusively declare ergogenic or ergolytic potential in athletes are lacking. The ability of cannabis and THC to perturb cardiovascular homeostasis warrants further investigation regarding mechanisms by which performance may be affected across different exercise modalities and energetic demands. In contrast to cannabis and THC, CBD has largely been scrutinized for its potential to aid in recovery. The beneficial effects of CBD on sleep quality, pain, and mild traumatic brain injury may be of particular interest to certain athletes. However, research in each of these respective areas has yet to be thoroughly investigated in athletic populations. Elucidating the effects of whole cannabis, THC, and CBD is pertinent for both researchers and practitioners given the widespread use of these products, and their potential to interact with athletes’ performance and recovery.

Adipose tissue (AT)-derived factors contribute to the regulation of cardiovascular homeostasis, thereby playing an important role in cardiovascular health and disease. In obesity, AT expands and becomes dysfunctional, shifting its secretory profile towards a pro-inflammatory state associated with deleterious effects on the cardiovascular system. AT in distinct locations (i.e., adipose depots) differs in crucial phenotypic variables, including inflammatory and secretory profile, cellular composition, lipolytic activity and gene expression. Such heterogeneity among different adipose depots may explain contrasting cardiometabolic risks associated with different obesity phenotypes. In this respect, central obesity, defined as the accumulation of AT in the abdominal region leads to higher risk of cardio-metabolic alterations compared to the accumulation of AT in the gluteofemoral region (i.e., peripheral obesity). The aim of this review is to provide updated summary of clinical and experimental evidence supporting the differential roles of different adipose depots in cardiovascular disease and to discuss the molecular basis underlying the differences of adipose depots in the regulation of cardiovascular function.

Today, cardiovascular diseases, due to their widespread prevalence, are among the most relevant biomedical problems in the modern world. The development of cardiovascular comorbidity among patients with diabetes mellitus is of high clinical urgency. Therefore, the study of cardiovascular risk modification among patients with diabetes mellitus is of paramount importance. In the context of the above, the data on the cardiotoxicity of fructose look very alarming since these patients usually use fructose as an affordable alternative to glucose. At the same time, it is an independent inducer of destabilization of cardiovascular homeostasis. Sixty rats were used in the experiment to study this problem. Modeling of fructose-induced overload was performed using a diabetic fructose supplement in an aqueous solution. The collection of herbs "Diabefit" was used as an infusion in addition to feeding highly enriched with fructose. The used markers which reflect the state of the heart and the blood vessels were: MDA, SOD, NO, and ET-1. MDA, ET-1, and NO concentrations demonstrated a significant increase in the fructose overload group and a significant decrease in the Diabefit group. At the same time, changes in SOD level as an indicator of the antioxidant reserve, on the contrary, implied a decrease in the group with a high fructose content and increased in the Diabefit group. All detected changes were associated with fructose-induced inhibition of SOD activity and its restoration using the Diabefit phyto-collection.

Vasopressin is involved in cardiovascular homeostasis that can influence coronary perfusion. It is commonly used as a local vasoconstricting agent during gynaecological procedures. We present a case of cardiac arrest and inverse Takotsubo features following intramyometrial vasopressin administration during myomectomy. The patient was successfully resuscitated and recovered completely. Cardiac presentation was compatible with inverse Takotsubo cardiomyopathy that could have been triggered by high-dose vasopressin-induced coronary vasoconstriction. The patient's cardiac function resolved with no long-term sequelae. Takotsubo cardiomyopathy usually results from an excessive catecholaminergic surge. High-dose vasopressin-induced coronary vasospasm could have been the mechanism underlying the clinical presentation in our patient. Learning points Local vasopressin administration during gynaecological procedures can result in rare but severe cardiovascular compromise.Takotsubo cardiomyopathy can result from multiple rare causes.High-dose vasopressin may cause Takotsubo cardiomyopathy features via coronary vasoconstriction.

Highlights • Exercise training is beneficial to the cardiovascular system. • Autophagy is critical in maintaining cardiovascular homeostasis and function. • Excessive or insufficient autophagy or autophagic flux can lead to cardiovascular disease. • Exercise-mediated bidirectional regulation of autophagy can prevent cardiovascular diseases., Cardiovascular disease is the leading cause of human death worldwide. Autophagy is an evolutionarily conserved degradation pathway, which is a highly conserved cellular degradation process in which lysosomes decompose their own organelles and recycle the resulting macromolecules. Autophagy is critical in maintaining cardiovascular homeostasis and function, and excessive or insufficient autophagy or autophagic flux can lead to cardiovascular disease. Enormous evidence indicates that exercise training plays a beneficial role in the prevention and treatment of cardiovascular diseases. The regulation of autophagy during exercise is a bidirectional process. For cardiovascular disease caused by either insufficient or excessive autophagy, exercise training restores normal autophagy function and delays the progression of cardiovascular disease. An in-depth exploration and discussion of exercise-mediated regulation of autophagy in the cardiovascular system can broaden our view about the prevention of various autophagy-related diseases through exercise training. In this article, we review autophagy and its related signaling pathways, as well as autophagy-dependent beneficial effects of exercise in cardiovascular system., Graphical abstract Image, graphical abstract

Purpose: Endoglin is a transmembrane glycoprotein which plays an important role in maintaining cardiovascular homeostasis. One of its forms, soluble endoglin (sEng), a molecule with antiangiogenic properties, has been found overexpressed in patients suffering from hypercholesterolemia, diabetes mellitus and hypertension, and is proposed as a marker of endothelial damage. Accordingly, we aimed to quantify the efficacy of various antihypertensive regimens on sEng levels, in hypertensive patients with endothelial dysfunction. Patients and methods: 323 patients were enrolled, and there were 99 patients with normal blood pressure values, 106 hypertensive patients under chronic treatment with different types of antihypertensive molecules (beta blockers, calcium channel blockers, and diuretics) in monotherapy, and 118 hypertensive patients under chronic treatment with perindopril. sEng plasma levels were quantified and were correlated with classical methods of assessing the endothelial damage. Results: Patients under chronic treatment with perindopril had lower sEng plasma levels compared with the other group of hypertensive patients under different regimens of antihypertensive treatment (sEng: 4.73±1.39 versus 5.63±2.33, p

Worldwide > 140 million people are living at high altitude and large numbers of lowlanders travel to high altitude for professional reasons or leisure activities. While there is widely held belief that sleep is perturbed at high altitude, little scientific evidence supports this notion. Here, we summarize recent work on sleep at high altitude in newcomers and high-altitude dwellers with particular emphasis on the interactions between sleep-disordered breathing (SDB) and cardiovascular regulation. Recent studies show an interaction between SDB and cardiovascular homeostasis in high-altitude dwellers. In high-altitude dwellers, SDB is associated with pulmonary hypertension and right ventricular dysfunction, premature atherosclerosis in the systemic circulation, and altered regulation of the cerebrovascular circulation related with cognitive decline and depression. In high-altitude dwellers, recent studies show a potential role of SDB in promoting cardiovascular morbidity and mortality. There is an urgent need for studies examining the effects of the treatment of SDB on cardiovascular homeostasis and its long-term benefits on cardiovascular morbidity/mortality in high-altitude dwellers.

Cardiovascular diseases are a major cause of death and disability. Despite enormous progress in diagnosis, prevention, and treatment over the years, the incidence of this group of pathologies continues to increase worldwide. An important step in reversing this situation is filling in the gaps we have in our understanding of cardiovascular homeostasis and of the pathogenic processes leading to disease. On this point, the discovery of epigenetics - heritable chemical modifications of DNA bases and histone proteins, as well as non-coding RNA-based mechanisms regulating gene expression - has opened up new vistas. Here, we will review recent findings regarding the epigenetics of three main vascular diseases (atherosclerosis, restenosis, and aortic aneurysm), with a focus on DNA methylation and histone modification. The emerging fundamental nature of epigenetics for cardiovascular physiopathology and, importantly, the amenability to manipulation with pharmacological techniques are an indication that epigenetics-based prognostic and therapeutics procedures might be developed in the future.

Despite the dynamic progress of modern medicine, oncological and cardiovascular diseases (CVD) remain a severe economic burden worldwide. Therefore, the study of chemotherapeutic cardiotoxicity appears to be comprehensively demanded. Nowadays, pharmacological therapy in oncology has undoubtedly unprecedented development, but at the same time, the rates of cardiovascular complications of chemotherapy still remain unchanged. The well-established and highly effective, but at the same time, cardiotoxic anthracyclines have not lost their relevance. Furthermore, they remain indispensable components of an immense amount of chemotherapy regimens, such as AC, FAC, etc. Moreover, the anthracycline-containing chemotherapy regimens have become a standard of care in several cancer types. In the context of the above mentioned, the study of the pathophysiological mechanisms, biochemical aspects, and dynamics of the morphological remodeling of doxorubicin-induced cardiovascular homeostasis disturbances will enable finding new targets of pharmacological therapy, which either in the short or long perspectives, will have a beneficial effect, improving both the quality of life and prognosis of oncological patients. This article covers a versatile overview of the molecular mechanisms of doxorubicin-induced cardiotoxicity. The pathogenesis of cardiotoxicity assessment could help to explore specific molecular mechanisms that initiate cardiovascular alteration that may favorably affect the future development of targeted drugs that could prevent cardiovascular events in cancer patients.

Endothelial NOS (eNOS), and its product NO, are vital components of the control of vasomotor function and cardiovascular homeostasis. In the present review, we will take a deep dive into eNOS enzymology, function and mechanisms regulating endothelial NO. The mechanisms regulating eNOS and NO synthesis discussed here include alterations to transcriptional, post-translational modifications and protein-protein regulations. Also, we will discuss the phenotypes associated with various eNOS mutants and the consequences of a disrupted eNOS/NO cascade, highlighting the importance of eNOS function and vascular homeostasis. LINKED ARTICLES: This article is part of a themed section on Nitric Oxide 20 Years from the 1998 Nobel Prize. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.2/issuetoc.

© 2018, Canadian Science Publishing. All rights reserved. The autonomic nervous system elicits continuous beat-by-beat homeostatic adjustments to cardiovascular control. These modifications are mediated by sensory inputs (e.g., baroreceptors, metaboreceptors, pulmonary, thermoreceptors, and chemoreceptors afferents), integration at the brainstem control centres (i.e., medulla), and efferent autonomic neural outputs (e.g., spinal, preganglionic, and postganglionic pathways). However, extensive electrical stimulation and functional imaging research show that the brain’s higher cortical regions (e.g., insular cortex, medial prefrontal cortex, anterior cingulate cortex) partake in homeostatic regulation of the cardiovascular system at rest and during exercise. We now appreciate that these cortical areas form a network, namely the “cortical autonomic network” (CAN), which operate as part of a larger central autonomic network comprising 2-way communication of cortical and subcortical areas to exert autonomic influence. Interestingly, differential patterns of CAN activity and ensuing cardiovascular control are present in disease states, thereby highlighting the importance of considering the role of CAN as an integral aspect of cardiovascular regulation in health and disease. This review discusses current knowledge on human cortical autonomic activation during volitional exercise, and the role of exercise training on this activation in both health and disease.