CPNE5 overexpression inhibits cardiomyocytes apoptosis by promoting the degradation of FAS receptor.

CPNE5, a member of the Copine family, is characterized by its membrane-binding properties and functions as a regulatory modulator of intracellular signaling through the spatial redistribution of interacting protein partners. Emerging evidence has demonstrated that CPNE3 exerts cardioprotective effects via anti-apoptotic activity in myocardial ischemia-reperfusion injury models. However, the functional role of CPNE5 in cardiac pathology remains unclear.

Nuclear Receptor ERRγ Protects Against Cardiac Ischemic Injury by Suppressing GBP5-Mediated Myocardial Inflammation.

Myocardial inflammation plays a critical role in the progression of injury following myocardial infarction (MI), yet the transcriptional mechanisms regulating cardiomyocyte inflammation to mitigate post-ischemic injury remain poorly understood. This study elucidated the role of Estrogen-Related Receptor Gamma (ERRγ) in modulating the inflammatory response post-MI, demonstrating that ERRγ expression was downregulated in ischemic tissue and hypoxic neonatal mouse ventricular myocytes (NMVMs). Cardiomyocyte-specific overexpression of ERRγ reduced infarct size, improved cardiac function, and suppressed excessive myocardial inflammation and pyroptosis by binding to the GBP5 promoter, thereby inhibiting GBP5 transcription and reducing NLRP3 inflammasome assembly.

Catheter ablation for persistent atrial fibrillation after acute decompensated heart failure Attack: Earlier is Better?

Background: Acute decompensated heart failure (ADHF) is often accompanied by persistent atrial fibrillation (AF). However, the optimal timing for RFCA in patients with persistent AF and ADHF is still uncertain.

Objectives: The aim of this observational cohort study is to investigate the safety and efficacy of early RFCA in patients with persistent AF after ADHF attack.