Mitochondria-Targeted Peptide Accelerates ATP Recovery and Reduces Ischemic Kidney Injury

• DOI: 10.1681/asn.2010080808
• Publication Date: 2011-05-06T03:07:09Z
• Authors: Hazel H. Szeto; Shaoyi Liu; Yi Soong; Dunli Wu; Shaun F. Darrah; Feng-Ying Cheng; Zhihong Zhao; Michael Ganger; Clara Y. Tow; Surya V. Seshan
• Keywords: Mitochondrial ROS

The burst of reactive oxygen species (ROS) during reperfusion ischemic tissues can trigger the opening mitochondrial permeability transition (MPT) pore, resulting in depolarization, decreased ATP synthesis, and increased ROS production. Rapid recovery upon is essential for survival tubular cells, inhibition oxidative damage limit inflammation. SS-31 a mitochondria-targeted tetrapeptide that scavenge inhibit MPT, suggesting it may protect against renal injury. Here, rat model ischemia-reperfusion (IR) injury, treatment with protected structure respiration early reperfusion, accelerated ATP, reduced apoptosis necrosis abrogated dysfunction. In addition, medullary vascular congestion, IR-mediated stress inflammatory response, proliferation surviving cells as 1 day after reperfusion. summary, these results support MPT an upstream target pharmacologic intervention IR injury protection function therapeutic maneuver to prevent necrosis, reduce stress, holds promise prevention acute kidney