The Emerging Role of m6A and Programmed Cell Death in Cardiovascular Diseases

Biomolecules, Journal Year: 2025, Volume and Issue: 15(2), P. 247 - 247

Published: Feb. 8, 2025

N6-methyladenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNA (mRNA), significantly impacting its lifecycle through dynamic and reversible processes involving methyltransferase, demethylase, binding proteins. These regulate mRNA stability, splicing, nuclear export, translation, degradation. Programmed cell death (PCD), a tightly controlled process encompassing apoptosis, pyroptosis, ferroptosis, autophagy, necroptosis, plays crucial role maintaining cellular homeostasis, tissue development, function. Recently, m6A has emerged as significant research area due to regulating PCD implications cardiovascular diseases (CVDs). In this review, we delve into intricate relationship between various types modification, emphasizing their pivotal roles initiation progression of CVDs such myocardial ischemia-reperfusion (I/R), atherosclerosis (AS), pulmonary hypertension (PH), cardiomyopathy, doxorubicin (Dox)-induced cardiotoxicity (DIC), heart failure (HF), infarction (MI). Our findings underscore potential elucidating CVD pave new pathways for prevention treatment strategies.

Language: Английский

Involvement of Oxidative Stress and Antioxidants in Modification of Cardiac Dysfunction Due to Ischemia–Reperfusion Injury

Antioxidants, Journal Year: 2025, Volume and Issue: 14(3), P. 340 - 340

Published: March 14, 2025

Delayed reperfusion of the ischemic heart (I/R) is known to impair recovery cardiac function and produce a wide variety myocardial defects, including ultrastructural damage, metabolic alterations, subcellular Ca2+-handling abnormalities, activation proteases, changes in gene expression. Although I/R injury has been reported induce formation reactive oxygen species (ROS), inflammation, intracellular Ca2+ overload, generation oxidative stress considered play critical role development dysfunction. Increases production superoxide, hydroxyl radicals, oxidants, such as hydrogen peroxide hypochlorous acid, occur hearts subjected injury. In fact, mitochondria are major source excessive ROS due impairment electron transport system well xanthine oxidase NADPH oxidase. Nitric oxide synthase, mainly present endothelium, also activated injury, leading nitric oxide, which, upon combination with superoxide generates nitrosative stress. Alterations function, sarcolemma, sarcoplasmic reticulum activities, mitochondrial phosphorylation, protease simulated exposing oxyradical-generating (xanthine plus oxidase) or H2O2. On other hand, endogenous antioxidants dismutase, catalase, glutathione peroxidase, concentration transcription factor (Nrf2), which modulates expression various antioxidants, depressed hearts. Furthermore, pretreatment catalase N-acetylcysteine, mercaptopropionylglycerine observed attenuate I/R-induced handling Ca2+-regulatory activities; additionally, it found depress improve function. These observations indicate that intimately involved pathological effects different alterations Thus, we faced task developing safe effective agents for upregulating therapy

Language: Английский

A comprehensive review of m6 A methylation in coronary heart disease

Journal of Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 10, 2025

Language: Английский