Ablation of mitophagy receptor FUNDC1 accentuates septic cardiomyopathy through ACSL4-dependent regulation of ferroptosis and mitochondrial integrity.

Sepsis evokes compromised myocardial function prompting heart failure albeit target therapy remains dismal. Our study examined the possible role of mitophagy receptor FUNDC1 in septic cardiomyopathy. A sepsis model was established using cecal ligation and puncture (CLP) in FUNDC1 knockout (FUNDC1) and WT mice prior to the evaluation of cardiac morphology, echocardiographic and cardiomyocyte contractile, oxidative stress, apoptosis, necroptosis, and ferroptosis.

Targeting ferroptosis in the maintenance of mitochondrial homeostasis in the realm of septic cardiomyopathy.

Septic cardiomyopathy is one of the predominant culprit factors contributing to the rising mortality in patients with severe sepsis. Among various mechanisms responsible for the etiology of septic heart anomalies, disruption of mitochondrial homeostasis has gained much recent attention, resulting in myocardial inflammation and even cell death. Ferroptosis is a novel category of regulated cell death (RCD) provoked by iron-dependent phospholipid peroxidation through iron-mediated phospholipid (PL) peroxidation, enroute to the rupture of plasma membranes and eventually cell death.

Cardiac-specific overexpression of catalase attenuates lipopolysaccharide-induced cardiac anomalies through reconciliation of autophagy and ferroptosis.

Lipopolysaccharide (LPS) from Gram-negative bacteria is a major contributor to cardiovascular failure, but the signaling mechanisms underlying its stress response are not fully understood. This study aimed to investigate the effect of the antioxidant enzyme catalase on LPS-induced cardiac abnormalities and the mechanisms involved, with particular focus on the interplay between autophagy, ferroptosis, and apoptosis. Cardiac-specific catalase (CAT) overexpression and wild-type (WT) mice were stimulated with LPS (6 mg/kg, intravenous injection), and cardiac morphology and function were evaluated.

Cardiac Glycoside Ouabain Exerts Anticancer Activity Downregulation of STAT3.

Cardiac glycosides are plant-derived steroid-like compounds which have been used for the treatment of cardiovascular diseases. Ouabain, a cardiotonic steroid and specific Na/K-ATPase inhibitor, has been rediscovered for its potential use in the treatment of cancer. However, the cellular targets and anticancer mechanism of ouabain in various cancers remain largely unexplored.