Myofibrillogenesis Regulator 1 Rescues Renal Ischemia/Reperfusion Injury by Recruitment of PI3K-Dependent P-AKT to Mitochondria

摘要: To investigate whether myofibrillogenesis regulator 1 (MR-1) attenuates renal ischemia/reperfusion (I/R) injury via inhibiting phosphorylated Akt (p-Akt) mitochondrial translocation-mediated opening of the permeability transition pore (mPTP), we injected adenovirus containing MR-1 gene or its siRNAs to left kidney subcapsular areas Sprague-Dawley rats, which subsequently underwent experimental I/R injury. Renal functions and severity tubular were evaluated by serum creatinine blood urea nitrogen levels pathological scores. We also examined morphology functions. Total/p-Akt assessed western blot using cytosolic fractions cortex tissue, respectively. found that p-Akt decreased, increased after reperfusion. Subcapsular injection led higher expression in mitochondria/cytosol, inhibited mPTP opening, alleviated injury; upregulated total more prominently compared with normal saline (NS) group. significantly lowered induced injury, damage, similar interacted homogenate. Wortmannin, a phosphatidylinositol 3 kinase (PI3K) inhibitor, abolished both recruitment protective effect overexpression on conclude, protects against through maintaining integrity, PI3K-dependent mitochondria. could be new therapeutic strategy for