Mitochondrial dysfunction on acute myocardial infarction or MDMA poisoning

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293162
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Legal medicine
• Research Institution: Kyoto Prefectural University of Medicine (2014-2015); The University of Tokyo (2013)
• Principal Investigator: Shintnai-Ishida Kaori (石田香) 京都府立医科大学, 医学(系)研究科(研究院), 准教授 (50345047)
• Co-Investigator(Kenkyū-buntansha): INUI Makoto 山口大学, 大学院医学系研究科, 教授 (70223237)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 急性心筋梗塞 / ＭＤＭＡ / ミトコンドリア / カルパイン / オートファジー

Outline of Final Research Achievements

The aims of this study was to clarify the molecular mechanisms of cardiac dysfunction, especially of mitochondria dysfunction, on acute myocardial infarction or a designer drug MDMA poisoning, and new findings were as follow;
1. Mitochondria of both rat and human cardiomyocytes have a calcium-dependent protease caplain. Acute myocardial infarction-activated mitochondrial calpain cleaves mitochondrial functional proteins, resulting in cardiac dysfunction.
2. In rat heart, MDMA causes lysosome destabilization following activation of the autophagy-lysosomal pathway, through which released lysosomal proteases damage myofibrils and induce cardiac dysfunction.

Free Research Field

法医学