AdipoRon ameliorates chronic ethanol induced cardiac necroptosis by reducing ceramide mediated mtROS.

Chronic ethanol (EtOH) consumption has been widely recognized as a significant contributor to cardiotoxicity. However, no specific treatment is currently available to ameliorate chronic ethanol induced cardiotoxicity. Adiponectin receptor agonist AdipoRon exerts protective effects in multiple organs through alleviating lipotoxicity.

Chronic ethanol exposure induces cardiac fibroblast transdifferentiation via ceramide accumulation and oxidative stress.

Aims: Excessive alcohol consumption is associated with cardiac dysfunction and the development of myocardial fibrosis. In this study, we aimed to investigate the direct impacts of ethanol on myocardial fibroblasts and elucidate the underlying mechanism responsible for chronic ethanol-induced myocardial fibrosis.

Methods: Rat primary cardiac fibroblasts exposed to ethanol for 24 h and C57BL/6J mice fed on Lieber-DeCarli diet to establish an ethanol intoxication model in vitro and in vivo, respectively.

Inhibition of Ceramide Synthesis Attenuates Chronic Ethanol Induced Cardiotoxicity by Restoring Lysosomal Function and Reducing Necroptosis.

Aims: Chronic alcohol misuse could cause alcoholic cardiomyopathy (ACM), and the specific mechanisms remained largely unknown. In this study, we aimed to explore the effects of endogenous ceramides on chronic ethanol-induced myocardial injury or cell loss (e.g.

Diagnostic Value of PICP and PIIINP in Myocardial Fibrosis: A Systematic Review and Meta-analysis.

Myocardial fibrosis is the excessive accumulation of extracellular matrix (ECM) components such as collagen and fibronectin, and its clinical diagnosis is always with limitations. Recently, PICP and PIIINP have been reported by several studies as potential biomarkers for the diagnosis of myocardial fibrosis, however, no meta-analyses focusing on the diagnostic values of these biomarkers have been conducted. So, the present study aimed to investigate the clinical diagnostic value of PICP and PIIINP in myocardial fibrosis patients.

Comprehensive analysis of transcriptomics and metabolomics to understand chronic ethanol induced murine cardiotoxicity.

Alcohol abuse has attracted public attention and long-term alcohol exposure can lead to alcohol-featured non-ischemic dilated cardiomyopathy. However, the precise underlying mechanisms of alcoholic cardiomyopathy remain to be elucidated. This study aimed to comprehensively characterize alcohol abuse-mediated effects on downstream metabolites and genes transcription using a multi-omics strategy.

Ethanol potentiates mirtazapine-induced cardiotoxicity by inducing dysfunctional autophagy via HMGB1-dependent Akt/mTOR signaling pathway.

Previous surveys have revealed that mirtazapine (MIR), one of the most commonly prescribed antidepressants, is associated with a higher risk of adverse cardiac events compared with other newer antidepressants. Chronic ethanol (EtOH) abuse could also lead to myocardial injuries. Concerning the common comorbidity of major depression and alcohol dependence, combined consumption of MIR and EtOH might be prevalent in patients with depression, resulting in an additive or synergistic cardiotoxic effect.

Abnormally High Blood Acetaldehyde Concentrations Suggest Potential Postmortem Ethanol Generation.

Ethanol is one of the most commonly used and abused substances worldwide. Identifying whether the source of ethanol detected in corpses is antemortem ingestion or postmortem generation is especially important for determining the cause of death, which remains a vibrant field of research. During the synthesis of ethanol in the putrefaction process of corpses, other small molecules such as acetaldehyde and n-propanol could also be produced.