Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning-Reference-Cited by-同舟云学术

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Lack of Contribution of p66shc and Its Mitochondrial Translocation to Ischemia-Reperfusion Injury and Cardioprotection by Ischemic Preconditioning

Published:2017-10-05 Issue: Volume:8 Page:
ISSN:1664-042X
Container-title:Frontiers in Physiology
language:
Short-container-title:Front. Physiol.

Author:

Boengler Kerstin,Bencsik Péter,Palóczi János,Kiss Krisztina,Pipicz Márton,Pipis Judit,Ferdinandy Péter,Schlüter Klaus-Dieter,Schulz Rainer

Publisher

Frontiers Media SA

Subject

Physiology (medical),Physiology

Reference43 articles.

1. Genetic deletion of the adaptor protein p66Shc increases susceptibility to short-term ischaemic myocardial injury via intracellular salvage pathways;Akhmedov;Eur. Heart J.,2015

2. Mitochondrial oxidative metabolism and uncoupling proteins in the failing heart;Akhmedov;Heart Fail. Rev.,2015

3. Mitochondrial oxygen radical generation and leak: sites of production in states 4 and 3, organ specificity, and relation to aging and longevity;Barja;J. Bioenerg. Biomembr.,1999

4. The p66ShcA adaptor protein regulates healing after myocardial infarction;Baysa;Basic Res. Cardiol.,2015

5. The gap junction modifier ZP1609 decreases cardiomyocyte hypercontracture following ischaemia/reperfusion independent from mitochondrial connexin 43;Boengler;Br. J. Pharmacol.,2017

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