The Mitochondria: A Target of Polyphenols in the Treatment of Diabetic Cardiomyopathy

International Journal of Molecular Sciences

AssaadA. Eid¹  Firas Kobeissy²  Gianfranco Pintus³  SuzanneA. Nasser⁴  AliH. Eid⁵  Humna Bhagani⁵  Ali Dakroub⁵  AhmedF. El-Yazbi⁵ 

[1] Department of Anatomy, Cell and Physiological Sciences, American University of Beirut, Beirut 11-0236, Lebanon;Department of Biochemistry and Molecular Genetics, American University of Beirut, Beirut 11-0236, Lebanon;Department of Medical Laboratory Sciences, University of Sharjah, Sharjah 27272, UAE;Department of Pharmacology and Therapeutics, Beirut Arab University, Beirut 11-5020, Lebanon;Department of Pharmacology and Toxicology, American University of Beirut, Beirut 11-0236, Lebanon;

关键词: diabetic cardiomyopathy;    polyphenols;    resveratrol;    autophagy;   

DOI  :  10.3390/ijms21144962

来源: DOAJ

【 摘 要 】

Diabetic cardiomyopathy (DCM) is a constellation of symptoms consisting of ventricular dysfunction and cardiomyocyte disarray in the presence of diabetes. The exact cause of this type of cardiomyopathy is still unknown; however, several processes involving the mitochondria, such as lipid and glucose metabolism, reactive oxygen species (ROS) production, apoptosis, autophagy and mitochondrial biogenesis have been implicated. In addition, polyphenols have been shown to improve the progression of diabetes. In this review, we discuss some of the mechanisms by which polyphenols, particularly resveratrol, play a role in slowing the progression of DCM. The most important intermediates by which polyphenols exert their protective effect include Bcl-2, UCP2, SIRT-1, AMPK and JNK1. Bcl-2 acts to attenuate apoptosis, UCP2 decreases oxidative stress, SIRT-1 increases mitochondrial biogenesis and decreases oxidative stress, AMPK increases autophagy, and JNK1 decreases apoptosis and increases autophagy. Our dissection of these molecular players aims to provide potential therapeutic targets for the treatment of DCM.

【 授权许可】

Unknown