These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Myocardial redox status, mitophagy and cardioprotection: a potential way to amend diabetic heart?
    Author: Bai T, Wang F, Zheng Y, Liang Q, Wang Y, Kong J, Cai L.
    Journal: Clin Sci (Lond); 2016 Sep 01; 130(17):1511-21. PubMed ID: 27433024.
    Abstract:
    Diabetic cardiomyopathy (DCM) is one of the major cardiovascular complications in diabetes that increase the mortality of diabetic patients. Mechanisms underlying DCM have not been fully elucidated, hindering targeted design of effective strategies to delay or treat DCM. Mitochondrial dysfunction is recognized as the driving force for the pathogenesis of DCM; therefore, maintaining cardiac mitochondrial quality is crucial for DCM prevention. Mitophagy is the process by which cells degrade abnormal or superfluous mitochondria in order to correct mitochondrial dysfunction, improve mitochondrial quality and maintain cardiac homoeostasis. Although the roles of mitophagy in various cardiomyopathies have been suggested, it remains largely unknown how the process is regulated and whether it is altered in the diabetic heart. In this review, we summarize currently available studies that investigate mitophagy in the heart, including its pathways, features and protective roles in several situations, including DCM. Due to limited data about mitophagy in diabetic hearts, future studies are required to gain a deeper understanding of the regulatory mechanisms of mitophagy in the heart and to develop mitophagy-based strategies for protecting the heart from diabetic injury.
    [Abstract] [Full Text] [Related] [New Search]