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Background: Black garlic is obtained from raw garlic (Allium sativum L.), by a fermentation process, under humidity and heat treatment, showing a high concentration of organosulfur compounds, which have been related to benefits in the prevention or delay of cardiovascular diseases (CVDs). The objective of the research was to evaluate whether long-term consumption of black garlic improves endothelial function and lipid profile in subjects with hypercholesterolemia. Methods: Single center, controlled clinical trial with two branches: Hypercholesterolemia vs. Healthy condition. Sixty-two subjects of both sexes were distributed in two groups, the hypercholesterolemia group (n = 31) (total cholesterol (TC) range 200–300 mg/dL and low-density lipoprotein (LDL)-cholesterol range 135–175 mg/dL) and the healthy group (n = 31). The intervention consisted of the ingestion of 4 cloves of black garlic (12 g) daily for 12 weeks. Results: significant increases in Apolipoprotein (Apo)A1 occurred in both groups: Hypercholesterolemia (Δ 11.8 mg/dL p < 0.001) vs Healthy (Δ 11.1 mg/dL p < 0.001). Besides, significant reductions for endothelial adhesion molecules monocyte chemoattractant protein-1 (MCP-1) (Δ −121.5 pg/mL p = 0.007 vs. Δ −56.3 pg/mL p = 0.015), intracellular adhesion molecule-1 (ICAM-1) (Δ −39.3 ng/mL p < 0.001 vs. Δ 63.5 ng/mL p < 0.001), and vascular cyto-adhesion molecule-1 (VCAM-1) (Δ −144.4 ng/mL p < 0.001 vs. Δ −83.4 ng/mL p = 0.061) were observed, for hypercholesterolemic and healthy subjects, respectively. Conclusions: These data show that black garlic consumption could improve some parameters related to endothelial function and lipid profile, which may have a favorable impact on the risk of CVDs, although more long-term studies are necessary to confirm. [ABSTRACT FROM AUTHOR]

BackgroundSerum carcinoembryonic antigen (CEA) is a biomarker commonly used to detect colorectal cancer. CEA levels are affected by many factors, including cardiometabolic diseases, such as cardiovascular diseases (CVDs) and diabetes. Cardiometabolic diseases and cancer share a similar pathological inflammatory pathway, which correlates with an unhealthy lifestyle. Hence, establishing an adequate CEA cut-off value might be a valuable reference for developing precision healthcare programs for cardiometabolic disease prevention. This study aimed to investigate the association between cardiometabolic risks and serum CEA and the underlying factors.MethodsA community-based, cross-sectional study was conducted between March and December 2021 on the western coast of Taiwan. Lifestyle data were assessed using a structured questionnaire. The cardiometabolic biomarkers, serum CEA, urine malondialdehyde, and 1-hydroxypyrene were quantified by the central laboratory of the collaborating hospital. Chi-square and binary multivariable logistic regression implemented in R version 4.0.2 were used to identify factors defining the risk of high serum CEA levels.ResultsA total of 6,295 adult residents without cancer-related diseases completed the study. The mean age was 48.6 (SD = 16.4) years, 56% were female, 32% had metabolic syndrome, and 23% and 10% had CVDs and diabetes, respectively. Multivariate logistic regression showed that age ≥ 65 years, male sex, alcohol consumption, smoking, infrequent use of dental floss, fewer remaining teeth, CVDs, diabetes, and oxidative stress were significantly associated with serum CEA ≥ 3 ng/mL. The discriminatory performance of the area under the receiver operating characteristic curve was 0.75 (0.73–0.76), showing that this model was suitable for distinguishing high CEA levels.ConclusionOur findings highlight the importance of understanding cardiometabolic diseases, unhealthy lifestyles, and oxidative stress, which contribute to high serum CEA. This study demonstrates that CEA, a well-known tumor marker, can help the early detection and prevention of cardiometabolic diseases via personalized lifestyle modification.

Cardiometabolic diseases (CMDs) are metabolic diseases (e.g., obesity, diabetes, atherosclerosis, rare genetic metabolic diseases, etc.) associated with cardiac pathologies. Pathophysiology of most CMDs involves increased production of reactive oxygen species and impaired antioxidant defense systems, resulting in cardiac oxidative stress (OxS). To alleviate OxS, various antioxidants have been investigated in several diseases with conflicting results. Here we review the effect of CMDs on cardiac redox homeostasis, the role of OxS in cardiac pathologies, as well as experimental and clinical data on the therapeutic potential of natural antioxidants (including resveratrol, quercetin, curcumin, vitamins A, C, and E, coenzyme Q10, etc.), synthetic antioxidants (including N-acetylcysteine, SOD mimetics, mitoTEMPO, SkQ1, etc.), and promoters of antioxidant enzymes in CMDs. As no antioxidant indicated for the prevention and/or treatment of CMDs has reached the market despite the large number of preclinical and clinical studies, a sizeable translational gap is evident in this field. Thus, we also highlight potential underlying factors that may contribute to the failure of translation of antioxidant therapies in CMDs. [Display omitted] • Oxidative stress (OxS) contributes to cardiac dysfunction in cardiometabolic diseases (CMDs). • Natural and synthetic antioxidants were shown to attenuate cardiac OxS in CMDs in animal studies. • Efficacy of antioxidants are controversial in clinical studies in CMD patients evidencing a translational gap. • Preclinical and clinical methodologies need improving to be able to establish therapeutic potential of antioxidants in CMDs. [ABSTRACT FROM AUTHOR]

Cardiometabolic diseases (CMDs) are currently the leading cause of death and disability worldwide, and their underlying regulatory mechanisms remain largely unknown. N6-methyladenosine (m6A) methylation, the most common and abundant epigenetic modification of eukaryotic mRNA, is regulated by m6A methyltransferase, demethylase, and the m6A binding protein, which affect the transcription, cleavage, translation, and degradation of target mRNA. m6A methylation plays a vital role in the physiological and pathological processes of CMDs. In this review, we summarize the role played by m6A methylation in CMDs, including obesity, hypertension, pulmonary hypertension, ischemic heart disease, myocardial hypertrophy, heart failure, and atherosclerosis. We also describe mechanisms that potentially involve the participation of m6A methylation, such as those driving calcium homeostasis, circadian rhythm, lipid metabolism, autophagy, macrophage response, and inflammation. m6A methylation and its regulators are expected to be targets for the treatment of CMDs.

• Metrnl could play a role in the occurrence of metabolic syndrome (MetS). • For sure, Metrnl is involved in metabolic turbulences; however, it is still far from a clinical biomarker in human diseases, and could be a therapeutic target in MetS. • Metrnl is an exercise mediator against metabolic conditions like T2D. • Exercise-induced Metrnl protective effects on heart diseases needs to be elucidated in humans. • Elucidation the role of other exercise-induced skeletal muscle's stressors like hypoxia and oxidative in Metrnl production other than exercise-induced muscle damage seems to be of great importance in the future. Metrnl is a secreted protein able to activate different intracellular signaling pathways in adipocytes, macrophages, myocytes and cardiomyocytes with physiological effects of the browning of white adipose tissue (BWT), insulin sensitivity, inflammation inhibition, skeletal muscle regeneration and heart protection. Shown to be regulated by obesity, diabetes, caloric restriction, weight loss and heart diseases, Metrnl is definitely involved in metabolic turbulences, and may play roles in metabolic syndrome (MetS). However, due to the conflicting data yielded, Metrnl is still far from clinical application as a diagnostic and/or a therapeutic agent or even a therapeutic target in MetS-related diseases such as type 2 diabetes (T2D) and obesity. Nevertheless, blood Metrnl levels as well as Metrnl as a cardiokine have been reported to play cardioprotective roles against heart diseases. Considering the established metabolic and anti-inflammatory hallmarks, exercise-induced Metrnl (as a myokine) is regarded as an exercise mediator in improving obesity-induced complications such as insulin resistance, T2D and inflammation. Besides, due to its healing role in muscle damage, Metrnl is also a potential therapeutic candidate to enhance regeneration with ageing or other inflammatory myopathies like Duchenne muscular dystrophy (DMD). Therefore, there are still many exercise-related questions unanswered on Metrnl, such as Metrnl-mediated fat browning in humans, exercise effects on heart Metrnl production and secretion and the effects of other exercise-induced skeletal muscle stressors like hypoxia and oxidative in Metrnl production other than exercise-induced muscle damage. [ABSTRACT FROM AUTHOR]