Physiological consequences of complex II inhibition for aging, disease, and the mKATP channel.

Andrew P Wojtovich, C Owen Smith, Cole M Haynes, Keith W Nehrke, Paul S Brookes

Journal: Biochimica et biophysica acta 2013;1827(5):598-611

PMID: 23291191

Free Full Text on Elsevier Science View on PubMed

Abstract

In recent years, it has become apparent that there exist several roles for respiratory complex II beyond metabolism. These include: (i) succinate signaling, (ii) reactive oxygen species (ROS) generation, (iii) ischemic preconditioning, (iv) various disease states and aging, and (v) a role in the function of the mitochondrial ATP-sensitive K(+) (mKATP) channel. This review will address the involvement of complex II in each of these areas, with a focus on how complex II regulates or may be involved in the assembly of the mKATP. This article is part of a Special Issue entitled: Respiratory complex II: Role in cellular physiology and disease.

Address: Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA.

DOI: 10.1016/j.bbabio.2012.12.007

Link outs

Free resources

Full Text Sources:

Medical:

https://medlineplus.gov/olderadulthealth.html

Other Literature Sources:

MeSH Terms: Adenosine Triphosphate, Aging, Electron Transport Complex II, Humans, Models, Biological, Mutation, Neoplasms, Physiological Phenomena, Potassium Channels