TL;DR
This study identifies RNF10 as a critical regulator of cardiac mitophagy, suggesting that targeting cardiac RNF10 may represent a therapeutic strategy for treating cardiac pathologies.
A cardiac-specific Miro1 knockout mouse model is generated to investigate how cardiomyocyte-Miro1 deficiency affects cardiac and mitochondrial structure-function and identifies Miro1 as a regulator of mitochondrial morphology.
Pathological cardiac hypertrophy is maladaptive cardiac remodeling induced by chronic adverse stimuli. In this study, the E3 ubiquitin ligase RNF128 was identified as a suppressor of pathological cardiac dysfunction with therapeutic value. Methods The expression of Ring Finger protein 128 (RNF128) in pathological cardi...
Claudin-5 (Cldn5) is traditionally recognized as a key component of endothelial tight junctions, however, its potential intracellular function within cardiomyocytes remains largely unexplored. This study aims to explore the molecular mechanisms underlying the cardioprotective role of Cldn5 on myocardial infarction (MI)...
Heart failure (HF) remains a leading cause of morbidity and mortality worldwide. A hallmark of HF progression is profound metabolic remodeling accompanied by mitochondrial dysfunction in cardiomyocytes. Impaired mitochondrial oxidative phosphorylation, excessive reactive oxygen species (ROS) production, and disrupted r...
Background: Protein quality control (PQC) is critical for maintaining sarcomere structure and function in cardiomyocytes. Mutations in PQC pathway proteins, namely CRYAB-R120G (arginine to glycine at position 120) and BAG3-P209L (proline to lysine at position 209) induce protein aggregates and cardiomyopathy in humans....
BACKGROUND Heart failure remains a leading cause of mortality globally, driven by persistent mitochondrial dysfunction and maladaptive cardiac hypertrophy. Although impaired autophagic flux contributes to cardiac deterioration, the precise molecular mechanisms are still unclear. The ubiquitin-proteasome system serves a...
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