Wei Deng

TL;DR: Investigation of the potential molecular mechanisms of STING in lipopolysaccharide (LPS)-induced cardiac injury using STING global knockout mice revealed that STING deficiency could alleviate LPS-induced SIC in mice, suggesting that targeting STing in cardiomyocytes may be a promising therapeutic strategy for preventing SIC.

TL;DR: It is concluded that ferritinophagy-mediated ferroptosis is one of the critical mechanisms contributing to sepsis-induced cardiac injury and Targeting ferroPTosis in cardiomyocytes may be a therapeutic strategy for preventing sepsi in the future.

TL;DR: Mechanistically, it was identified that FNDC5/Irisin activated AKT/mTOR signaling and decreased DOX-induced cardiomyocyte apoptosis, and moreover, direct evidence was provided that the anti-oxidant effect of F NDC5 / irisin was mediated by the AKT /GSK3β/FYN/Nrf2 axis in an mTOR-independent manner.

TL;DR: This review describes the key molecular and cellular responses involved in pathological cardiac remodelling, a precursor of clinical heart failure (HF).

TL;DR: Mechanistically, it is found that matrine ameliorated DOX-induced uncoupling protein 2 (UCP2) downregulation, and UCP2 inhibition by genipin could blunt the protective effect of matrine on DOx-induced oxidative stress and cardiomyocyte apoptosis, and it might be a promising therapeutic agent for the treatment of DOX -induced cardiotoxicity.