Format

Send to

Choose Destination
Trends Endocrinol Metab. 2015 Feb;26(2):75-83. doi: 10.1016/j.tem.2014.11.003. Epub 2014 Dec 9.

Poly(ADP-ribose) polymerases as modulators of mitochondrial activity.

Author information

1
Research Center for Molecular Medicine, University of Debrecen, Debrecen, Hungary; MTA-DE Lendület Laboratory of Cellular Metabolism Research Group, Debrecen, Hungary; Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary. Electronic address: baip@med.unideb.hu.
2
MTA-DE Lendület Laboratory of Cellular Metabolism Research Group, Debrecen, Hungary; Department of Medical Chemistry, University of Debrecen, Debrecen, Hungary.
3
Department of Intensive Care Medicine and Burn Center, Lausanne University Hospital Medical Center, Lausanne, Switzerland.
4
Laboratory Physiological Studies, Section on Oxidative Stress and Tissue Injury, NIH/NIAAA/DICBR, Bethesda, MD, USA.

Abstract

Mitochondria are essential in cellular stress responses. Mitochondrial output to environmental stress is a major factor in metabolic adaptation and is regulated by a complex network of energy and nutrient sensing proteins. Activation of poly(ADP-ribose) polymerases (PARPs) has been known to impair mitochondrial function; however, our view of PARP-mediated mitochondrial dysfunction and injury has only recently fundamentally evolved. In this review, we examine our current understanding of PARP-elicited mitochondrial damage, PARP-mediated signal transduction pathways, transcription factors that interact with PARPs and govern mitochondrial biogenesis, as well as mitochondrial diseases that are mediated by PARPs. With PARP activation emerging as a common underlying mechanism in numerous pathologies, a better understanding the role of various PARPs in mitochondrial regulation may help open new therapeutic avenues.

KEYWORDS:

AMP activated kinase; NAD(+); Sirtuin; hypoxia-inducible factor; nuclear respiratory factor; poly(ADP-ribose) polymerase

PMID:
25497347
DOI:
10.1016/j.tem.2014.11.003
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center