Open AccessPhosphorylation in Novel Mitochondrial Creatine Kinase Tyrosine Residues Render Cardioprotection against Hypoxia/Reoxygenation Injury
Author(s) -
Nammi Park,
Jubert Marquez,
Maria Victoria Faith Garcia,
Ippei Shimizu,
Sung Ryul Lee,
Hyoung Kyu Kim,
Jin Han
Publication year - 2021
Publication title -
journal of lipid and atherosclerosis
Language(s) - English
Resource type - Journals
eISSN - 2288-2561
pISSN - 2287-2892
DOI - 10.12997/jla.2021.10.2.223
Subject(s) - cardioprotection , microbiology and biotechnology , phosphorylation , biology , mitochondrion , viability assay , dephosphorylation , ischemic preconditioning , pharmacology , biochemistry , ischemia , medicine , cell , phosphatase
Ischemic cardiomyopathy (ICM) is the leading cause of heart failure. Proteomic and genomic studies have demonstrated ischemic preconditioning (IPC) can assert cardioprotection against ICM through mitochondrial function regulation. Considering IPC is conducted in a relatively brief period, regulation of protein expression also occurs very rapidly, highlighting the importance of protein function modulation by post-translational modifications. This study aimed to identify and analyze novel phosphorylated mitochondrial proteins that can be harnessed for therapeutic strategies for preventing ischemia/reperfusion (I/R) injury.