ROS-mediated PARP activity undermines mitochondrial function after permeability transition pore opening during myocardial ischemia-reperfusion.

Journal of the American Heart Association

Volumn 2, Issue 2, 2013, Pages

  Schriewer, Jacqueline M ^a   Peek, Clara Bien ^b   Bass, Joseph ^b   Schumacker, Paul T ^b  

^a NORTHWESTERN UNIVERSITY   (United States)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

CARRIER PROTEIN; CYCLOPHILIN; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; NICOTINAMIDE ADENINE DINUCLEOTIDE ADENOSINE DIPHOSPHATE RIBOSYLTRANSFERASE; PARP1 PROTEIN, MOUSE; REACTIVE OXYGEN METABOLITE;

ANIMAL; ARTICLE; CELL DEATH; CELL SURVIVAL; DISEASE MODEL; ENZYMOLOGY; GENETICS; HEART MITOCHONDRION; HEART MUSCLE ISCHEMIA; KNOCKOUT MOUSE; METABOLISM; MITOCHONDRIAL MEMBRANE; MITOCHONDRIAL MEMBRANE POTENTIAL; MOUSE; OXIDATIVE STRESS; PATHOPHYSIOLOGY; PHYSIOLOGY; REPERFUSION INJURY;

ANIMALS; CELL DEATH; CELL SURVIVAL; CYCLOPHILINS; DISEASE MODELS, ANIMAL; MEMBRANE POTENTIAL, MITOCHONDRIAL; MICE; MICE, KNOCKOUT; MITOCHONDRIA, HEART; MITOCHONDRIAL MEMBRANE TRANSPORT PROTEINS; MITOCHONDRIAL MEMBRANES; MYOCARDIAL ISCHEMIA; MYOCARDIAL REPERFUSION INJURY; OXIDATIVE STRESS; POLY(ADP-RIBOSE) POLYMERASES; REACTIVE OXYGEN SPECIES;

EID: 84884379434     PISSN: None     EISSN: 20479980     Source Type: None    
DOI: 10.1161/JAHA.113.000159     Document Type: Article

References (0)