ELA-11 protects the heart against oxidative stress injury induced apoptosis through ERK/MAPK and PI3K/AKT signaling pathways

• DOI: 10.3389/fphar.2022.873614
• Publication Date: 2022-09-08T05:08:09Z
• Authors: Xuejun Wang; Li Zhang; Mengwen Feng; Zhongqing Xu; Zijie Cheng; Lingmei Qian
• Keywords: Pharmacology; 0301 basic medicine; 03 medical and health sciences; apoptosis; heart failure; oxidative stress; Therapeutics. Pharmacology; RM1-950; doxorubicin; ELA-11; 3. Good health

Increasing evidence revealed that apoptosis and oxidative stress injury were associated with the pathophysiology of doxorubicin (DOX)-induced myocardial injury. ELABELA (ELA) is a newly identified peptide 32 amino acids, can reduce hypertension exogenous infusion. However, effect 11-residue furn-cleaved fragment (ELA-11) still unclear. We first administrated ELA-11 in DOX-injured mice measured cardiac function investigated vivo . found alleviated heart induced by DOX inhibited tissues from apoptosis. In vitro , regulated sensitivity towards treatment through PI3K/AKT ERK/MAPK signaling pathway. Similarly, stress-induced cobalt chloride (CoCl 2 )-injured cardiomyocytes. Moreover, protected cardiomyocyte interacting Apelin receptor (APJ) using 4-oxo-6-((pyrimidin-2-ylthio) methyl)-4H-pyran-3-yl 4-nitrobenzoate (ML221). Hence, our results indicated protective role DOX-induced