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Cuphea carthagenensis (Jacq.) J. F. Macbr. is a popular plant in Brazilian folk medicine owing to its hypotensive and central nervous system depressant effects. This study aimed to validate the hypotensive effect of the plantʼs aqueous extract (AE) in rats and examine the vascular actions of three hydrolyzable tannins, oenothein B, woodfordin C, and eucalbanin B, isolated from AE. Systolic blood pressure in unanesthetized rats was determined using the non-invasive tail-cuff method. Oral treatment of normotensive rats with 0.5 and 1.0 g/kg/day AE induced a dose-related hypotensive effect after 1 week. In rat aortic rings pre-contracted with noradrenaline, all ellagitannins (20 – 180 µM) induced a concentration-related vasorelaxation. This effect was blocked by either removing the endothelium or pre-incubating with NG-nitro- l -arginine methyl ester (10 µM), an inhibitor of nitric oxide (NO) synthase. In KCl-depolarized rat portal vein preparations, the investigated compounds did not affect significantly the maximal contractile responses and pD2 values of the concentration-response curves to CaCl2. Our results demonstrated the hypotensive effect of C. carthagenensis AE in unanesthetized rats. All isolated ellagitannins induced vasorelaxation in vitro via activating NO synthesis/NO release from endothelial cells, without altering the Ca2+ influx in vascular smooth muscle preparations. Considering the low oral bioavailability of ellagitannins, the determined in vitro actions of these compounds are unlikely to account for the hypotensive effect of AE in vivo. It remains to be determined the role of the bioactive ellagitannin-derived metabolites in the hypotensive effect observed after oral treatment of unanesthetized rats with the plant extract. [ABSTRACT FROM AUTHOR]

• A multifunctional dressing based on bacterial cellulose deposited with a tannic acid/Cu2+ ion/Mg2+ ion complex film (BTCM) is developed. • The BTCM membrane can effectively eradicate bacteria in the wound area under a short-term near-infrared irradiation. • The BTCM membrane can promote proliferation, migration, and tube formation of endothelial cells in vitro and angiogenesis in vivo. • The BTCM membrane can accelerate the healing process of the bacteria-infected full-thickness skin wounds. For most traditional wound dressings, it is challenging to simultaneously eliminate bacteria and promote angiogenesis to accelerate the healing process of bacteria-infected wounds. In this work, we develop a multifunctional dressing based on bacterial cellulose (BC) deposited with a tannic acid/Cu2+ ion/Mg2+ ion (TCM) complex film. Overall, the TCM complex exhibits robust interfacial adhesion to modify BC and good photothermal properties to effectively eradicate bacteria in the wound area under near-infrared (NIR) irradiation. The individual components of the TCM complex have several advantageous features for wound healing, such as antibacterial ability and negligible cytotoxicity; in particular, the released Cu2+ and Mg2+ ions are favorable for the proliferation, migration, and tube formation of endothelial cells in vitro. The results of in vivo experiments demonstrated that with the assistance of NIR irradiation, this composite dressing is more effective than traditional gauze or pristine BC dressing in promotion of angiogenesis and collagen deposition without causing remarkable inflammation, thereby accelerating the healing process of bacteria-infected full-thickness skin wounds. This work thus provides a simple and facile way to fabricate multifunctional BC-based dressings that could be potentially used for treating infected wounds. [Display omitted] [ABSTRACT FROM AUTHOR]

(−)-Epigallocatechin gallate (EGCG) is one of the autophagy stimulators that have been reported to protect vascular endothelial cells from oxidative stress-induced damage. In this study, we attempted potentiation of the autophagy-stimulating activity of EGCG in human aortic epithelial cells (HAECs) by using the EGCG-phenylalanine conjugate, E10. Autophagy-stimulating activity of E10 was evaluated by LC3-II measurement in the absence and presence of the lysosomal blocker chloroquine, CTYO-ID staining, and reporter assay using tandem fluorescence-tagged LC3. These experiments revealed significantly enhanced autophagic flux stimulation in HAECs by E10 compared with EGCG. Further elaboration of E10 showed that activation of AMPK through phosphorylation as the major mechanism of its autophagy stimulation. Like other autophagy stimulators, E10 protected HAECs from lipotoxicity as well as accompanying endothelial senescence. Finally, stimulation of autophagy by E10 was shown to protect HAECs from oxidative stress-induced apoptosis. These findings collectively suggest potential clinical implications of E10 for various cardiovascular complications through stimulation of autophagy. [ABSTRACT FROM AUTHOR]

A study conducted in Madrid, Spain, explored the role of NFkB-inducing kinase (NIK) in neointimal hyperplasia following endothelial cell injury. The research found that NIK deficiency led to reduced inflammation and stenosis in mice with endothelial cell injury compared to control mice. The study suggests that targeting NIK could be a potential therapeutic approach to limit arterial stenosis post-endothelial cell injury. [Extracted from the article]

Researchers at Henan University of Science and Technology conducted a study on tumor endothelial cells (TECs) in hepatocellular carcinoma (HCC) using single-cell sequencing and pseudotime analysis. The study identified two subgroups of TECs with distinct functional activities and signaling pathways, shedding light on their potential roles in tumor progression. The findings suggest new therapeutic targets and strategies for personalized treatment of HCC, emphasizing the importance of further exploring TECs heterogeneity in understanding the disease's molecular mechanisms. [Extracted from the article]

A recent study conducted at the University of Strasbourg explored the impact of plasma from patients with severe aortic stenosis on valvular endothelial cells. The research highlighted the detrimental effects of plasma from severe AS patients on aortic VECs, leading to increased oxidative stress and endothelial dysfunction. The study emphasized the role of FXa in promoting oxidative stress and contributing to valvular endothelial dysfunction. This research sheds light on potential therapeutic avenues for treating aortic stenosis, particularly in the context of transcatheter aortic valve replacement (TAVR). [Extracted from the article]

Researchers at Chongqing Medical University have reported new findings on thin basement membrane nephropathy, a kidney condition affecting the glomerular filtration barrier. The study identified five novel pathogenic FN1 mutations contributing to the condition, shedding light on its genetic pathogenesis. This research provides insights into potential therapeutic strategies and distinguishes TBMN from early-stage Alport syndrome, offering a crucial foundation for understanding renal dysfunction associated with hematuria. [Extracted from the article]

Researchers at the University of Macau have conducted a study on endothelial cells, focusing on the neuroprotective properties of a novel derivative called T-006. The research found that T-006 showed significant protective effects against oxidative injuries in both neuronal and endothelial cells by regulating specific signaling pathways. This study sheds light on potential mechanisms for improving cell survival and antioxidant defenses in conditions such as ischemic stroke and neurodegenerative diseases. The findings were published in the journal Antioxidants and can be accessed for further information. [Extracted from the article]

A study conducted at the University of Surrey focused on the safety, acceptability, and feasibility of isolating endothelial cells (EC) from discarded guidewires in patients undergoing major surgery or with acute critical illness. The research aimed to compare EC phenotypes in different patient cohorts and found that it is feasible to isolate ECs from patients during standard care procedures using discarded guidewires. The study concluded that isolating ECs from patients through this method is well-tolerated and carries low risk, providing valuable insights into the roles of ECs in health and disease. [Extracted from the article]

A recent study conducted at University Hospital Zurich explored the effects of BET inhibition on lung micro-environmental changes in obesity-related pulmonary arterial hypertension (PAH). The research highlighted the impact of obesity on vascular structure and function, as well as the potential therapeutic benefits of BET inhibitors in resetting the lung micro-environment to reduce inflammation and senescence. The study concluded that APA treatment could prevent PAH-related features in obese mice and influence fibroblast migration through direct and paracrine mechanisms. This research provides valuable insights into the molecular mechanisms underlying obesity-related PAH and potential treatment approaches. [Extracted from the article]

Researchers have submitted a patent application for a method using trigonelline to mitigate cardiomyopathy caused by the SARS-CoV-2 spike protein in obese patients. The application aims to prevent heart injuries by administering trigonelline to attenuate spike-protein exacerbated lipotoxicity and mitochondrial dysfunction in endothelial cells and cardiomyocytes. This method targets post-acute sequelae of COVID-19, particularly in patients with long COVID and heart problems, offering potential therapeutic benefits. [Extracted from the article]

The article discusses how leukocytes, specifically neutrophils, use endothelial membrane tunnels to extravasate from blood vessels during inflammation. The study found that endothelial cells form membrane tunnels that allow neutrophils to cross through the vessel walls. This discovery provides insight into the 3D multicellular architecture involved in the process of leukocyte transmigration. The research has not yet undergone peer review and can be accessed on biorxiv.org for further information. [Extracted from the article]

A recent study from Fudan University explores the impact of high uric acid on vascular endothelial cell injury through glycolytic inhibition. The research suggests that hyperuricemia can lead to reduced ATP production in endothelial cells by inhibiting the expression of key glycolytic enzymes. By investigating the XBP1-PKM2 signaling pathway, the study sheds light on potential mechanisms underlying endothelial cell injury and its implications for vascular health. This research provides valuable insights into the early stages of atherosclerosis and the importance of maintaining endothelial barrier integrity for vascular homeostasis. [Extracted from the article]

Researchers from the Faculty of Medicine and University Hospital Carl Gustav Carus in Dresden, Germany, have conducted a study on flavoproteins, specifically focusing on the NADPH oxidase isoform 4 (NOX4) and its role in endothelial function under hypoxia. The research found that NOX4 and prostaglandin I2 synthase (PTGIS) expression are closely correlated in occluded, hypoxic human vessels, with hypoxia significantly elevating their expression and activity in human endothelial cells. The study concluded that protective laminar blood flow can restore endothelial function and mitigate the hypoxic response on NOX4 and PTGIS, ensuring endothelium-dependent vasodilation under hypoxic conditions. [Extracted from the article]

New research from the Department of Pharmacology and Toxicology explores the impact of knocking out Sirtuin 3 in endothelial cells on vascular function in mice. The study found that Sirtuin 3 plays a crucial role in regulating endothelial-dependent relaxation and myogenic responses in distal intramural branches of arteries. The research suggests that endothelial Sirtuin 3 is essential for maintaining vascular function and blood flow autoregulation, with sex and organ-specific differences observed in the study. [Extracted from the article]

Researchers from the Research Institute for Complex Issues of Cardiovascular Diseases in Kemerovo, Russia, conducted a study on endothelial cells and their response to calciprotein particles (CPPs). The study used proteomic profiling to analyze the secretomes of endothelial cells treated with different particles. The findings indicated changes in the secretion of specific proteins, suggesting potential signs of endothelial dysfunction. This research provides valuable insights into the molecular mechanisms underlying endothelial cell responses to CPP exposure. [Extracted from the article]

Researchers from Soochow University in Jiangsu, China, conducted a study on the influence of the Nrg1/erbb4 signaling pathway on human pulmonary artery endothelial cells (HPAECs). The research found that ERBB4 levels were significantly higher in patients with pulmonary embolism compared to healthy controls. The study concluded that ERBB4 has the potential to be a novel biological marker of pulmonary embolism. For more information, readers can refer to the original article published in Pulmonary Circulation. [Extracted from the article]

The article discusses the impact of Plasmodium falciparum-infected red blood cells on brain endothelial cells, leading to changes in gene expression related to immune response, angiogenesis, and antiviral mechanisms. The study highlights how the presence of infected red blood cells activates immunological pathways and affects antiviral and angiogenesis processes in endothelial cells. The research emphasizes the induction of the interferon-alpha/beta signaling pathway in response to infected red blood cells, shedding light on the complex interactions between malaria parasites and host cells. [Extracted from the article]

The article discusses the spatiotemporal dynamics of primary and motile cilia during lung development. It highlights the varying roles of cilia in mammalian cells, such as transduction of signals and fluid flow generation. The study reveals that endothelial cells lack primary cilia, while the lung epithelium shows a gradient of ciliary distribution over time. Mesenchymal cells exhibit uniform ciliation in early development, with specific fibroblasts retaining cilia in adult alveoli. The research emphasizes the need to understand the spatiotemporal functions of cilia in different cellular populations. [Extracted from the article]

A recent study highlighted in Health & Medicine Week discusses the identification of HIF-2a as a potential therapeutic target for highly immune-infiltrated melanomas. The research focused on stratified analysis of patients treated with different immune-checkpoint blockade regimens, revealing that high immune infiltrate was a biomarker for response to combination ICB. Additionally, hypoxia-related signatures were associated with non-response to anti-PD-1 in immune infiltrate-high melanomas. The study emphasizes the importance of careful stratification by clinical and molecular characteristics in deriving meaningful biological insights for the development of novel clinical targets in cancer therapy. [Extracted from the article]

The article discusses the impact of hsa-miR-9-5p, found in syncytiotrophoblast-derived extracellular vesicles from early-onset preeclampsia, on the proangiogenic properties of brain endothelial cells. The study reveals that hsa-miR-9-5p reduces cell proliferation and migration in brain endothelial cells without affecting cell viability, potentially through the modulation of angiogenic regulators. These findings contribute to understanding cerebrovascular alterations in preeclampsia and may inform future research and therapeutic interventions. [Extracted from the article]

Researchers at Sapienza University of Rome conducted a study on hyperglycemia and its impact on endothelial dysfunction, a key factor in cardiovascular diseases. The study focused on the role of autophagy in vascular damage induced by diabetes and found that restoring autophagy can reduce diabetes-induced endothelial damage. The research suggests that targeting autophagy could be a promising therapeutic strategy to mitigate the cardiovascular effects of metabolic stress. The full study can be accessed in the European Heart Journal, published by Oxford University Press. [Extracted from the article]

A study conducted by the Karolinska Institute explored the impact of extracellular vesicles (EVs) derived from red blood cells (RBCs) on endothelial dysfunction in type 2 diabetes (T2D). The research found that EVs from T2D-RBCs were taken up by endothelial cells at a higher rate compared to healthy controls, leading to increased levels of arginase-1 and subsequent endothelial dysfunction. The study suggests that understanding the mechanism of EV uptake could pave the way for new treatment strategies in T2D management. [Extracted from the article]

A recent study from the University of Pittsburgh School of Medicine explores the role of Z-DNA binding protein 1 (ZBP1) in sepsis-induced acute lung injury (ALI). The research suggests that ZBP1 plays a crucial role in regulating macrophages and lung endothelial cells during sepsis, impacting inflammatory signaling pathways and cellular damage. These findings highlight ZBP1 as a potential therapeutic target for treating sepsis-induced ALI. For more information, the full article can be accessed in Communications Biology. [Extracted from the article]

A recent study conducted at University Hospital Bonn focused on the role of extracellular vesicle-incorporated long noncoding RNA PUNISHER in patients with coronary artery disease (CAD). The research found that PUNISHER levels were significantly increased in CAD patients compared to those without CAD, and its transfer via extracellular vesicles promoted a pro-angiogenic phenotype through a VEGFA-dependent mechanism. This study sheds light on the potential role of circulating lncRNAs in cardiovascular diseases and highlights the importance of understanding the molecular mechanisms underlying heart disease. [Extracted from the article]

The article discusses a patent issued to INSERM for the use of PI3KC2B inhibitors to preserve vascular endothelial cell barrier integrity in ischemic conditions. The patent inventors are from France and the UK, and the patent was filed in 2019 and published in 2024. The invention aims to address the damaging consequences of reperfusion following ischemic events, highlighting the need for new therapies to treat ischemia and ischemia-reperfusion injuries. [Extracted from the article]

Researchers from Shanghai University of Traditional Chinese Medicine have conducted a study on the relationship between homocysteine-induced vascular endothelial cell death and iron deficiency. The study found that intracellular iron deficiency and abnormal metabolism, rather than ferroptosis, contribute to this process. The research focused on the mechanisms underlying Hcy-induced vascular endothelial injury and iron metabolism dysfunction, highlighting the disruption of the intracellular antioxidant system and iron metabolism as key factors. This study provides valuable insights into the complex interplay between homocysteine, iron deficiency, and vascular health. [Extracted from the article]

Researchers at Capital Medical University have conducted a study on cerebral venous congestion (CVC) and its link to thrombosis, focusing on the cellular and molecular alterations in endothelial cells. The study found that CVC can induce endothelial cell damage, leading to a procoagulant phenotype and increasing the risk of cerebral venous thrombosis (CVT). This research sheds light on the pathophysiology of CVC and reexamines Virchow's triad in the context of CVC. For more information, the full article can be accessed for free at the Cell & Bioscience website. [Extracted from the article]

The article explores the endothelial features in chronic thromboembolic pulmonary hypertension (CTEPH), a rare complication of pulmonary embolism. It discusses the potential role of defective angiogenesis and altered pulmonary arterial endothelial cell function in disease progression. The study focuses on histological characteristics of the pulmonary vascular tree, specifically looking at angiogenic capacities and endothelial barrier function in pulmonary arterial lesions obtained during pulmonary endarterectomy. Despite differences in angiogenic cues between large and (sub)-segmental pulmonary arterial lesions, in vitro angiogenic capacities and barrier function of pulmonary arterial endothelial cells remain unchanged. [Extracted from the article]

Researchers from the Fraunhofer-Institute for Applied Polymer Research conducted a study on the effects of Arthrospira platensis (AP) on human umbilical vein endothelial cells to understand atherosclerosis better. The study found that AP increased cell proliferation without causing inflammation, promoting an antithrombotic state. This research suggests that AP could potentially be used to accelerate endothelial cell proliferation in conditions like atherosclerosis or after stent placement. For more information, the study can be found in Life journal, volume 14, issue 10. [Extracted from the article]

Research conducted at the University of Maryland focused on Hutchinson-Gilford progeria syndrome (HGPS), a rare premature aging disorder caused by a genetic mutation. The study found that Angiopoietin-2 (Ang2) plays a crucial role in reversing endothelial cell dysfunction in HGPS, potentially offering therapeutic benefits for cardiovascular diseases associated with the condition. The research, supported by the NIH National Heart Lung & Blood Institute, sheds light on the molecular mechanisms underlying HGPS-related cardiovascular pathology and highlights the potential of Ang2 treatment in addressing these issues. [Extracted from the article]

The article discusses the urgent need for additional therapeutic strategies for melanoma patients who do not respond to current treatments or develop resistance. A study was conducted to identify compounds that target drug-naive and -resistant melanoma cells, using a metabolism-oriented compound library in different cell culture media and growth conditions. The NAMPT inhibitor FK866 was found to be highly effective in suppressing melanoma cell growth without affecting healthy cells in 3D models. This research has not yet been peer-reviewed and more information can be found on biorxiv.org. [Extracted from the article]

The article discusses the impact of systemic inflammation on neuroinflammation, highlighting the role of the transcription factor Nrf2 in endothelial cells as a critical regulator of this process. The study found that activation of Nrf2 could prevent inflammatory reactions in the brain caused by peripheral inflammation. The research suggests that targeting endothelial cell Nrf2 could be a potential therapeutic approach to mitigate the adverse effects of systemic inflammation on the central nervous system. [Extracted from the article]