MOTS-c repairs myocardial damage by inhibiting the CCN1/ERK1/2/EGR1 pathway in diabetic rats

• DOI: 10.3389/fnut.2022.1060684
• Publication Date: 2023-01-04T19:47:41Z
• Authors: Manda Wang; Gangqiang Wang; Xiaoli Pang; Jiacheng Ma; Jinghan Yuan; Yanrong Pan; Yu Fu; Ismail Laher; Shunchang Li
• Keywords: Diabetic Cardiomyopathy

Cardiac structure remodeling and dysfunction are common complications of diabetes, often leading to serious cardiovascular events. MOTS-c, a mitochondria-derived peptide, regulates metabolic homeostasis by accelerating glucose uptake improving insulin sensitivity. Plasma levels MOTS-c decreased in patients with diabetes. can improve vascular endothelial function, making it novel therapeutic target for the We investigated effects on cardiac function analyzed transcriptomic characteristics diabetic rats. Our results indicate that treatment 8-week repaired myocardial mitochondrial damage preserved systolic diastolic function. Transcriptomic analysis revealed altered 47 disease causing genes. Functional enrichment indicated attenuated heart involved apoptosis, immunoregulation, angiogenesis fatty acid metabolism. Moreover, reduced apoptosis downregulating CCN1 genes thereby inhibiting activation ERK1/2 expression its downstream EGR1 gene. findings identify potential targets T2D cardiomyopathy.