Increase in Cardiac Ischemia-Reperfusion Injuries in Opa1+/- Mouse Model.

ABSTRACT:

Background

Recent data suggests the involvement of mitochondrial dynamics in cardiac ischemia/reperfusion (I/R) injuries. Whilst excessive mitochondrial fission has been described as detrimental, the role of fusion proteins in this context remains uncertain.

Objectives

To investigate whether Opa1 (protein involved in mitochondrial inner-membrane fusion) deficiency affects I/R injuries.

Methods and results

We examined mice exhibiting Opa1delTTAG mutations (Opa1+/-), showing 70% Opa1 protein expression in the myocardium as compared to their wild-type (WT) littermates. Cardiac left-ventricular systolic function assessed by means of echocardiography was observed to be similar in 3-month-old WT and Opa1+/- mice. After subjection to I/R, infarct size was significantly great

SUBMITTER: Le Page S 

PROVIDER: S-EPMC5056696 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature