Inducible Expression of BNIP3 Provokes Mitochondrial Defects and Hypoxia-Mediated Cell Death of Ventricular Myocytes

ABSTRACT—In this study, we provide evidence for the operation of BNIP3 as a key regulator of mitochondrial function and cell death of ventricular myocytes during hypoxia. In contrast to normoxic cells, a 5.6-fold increase (P

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Bibliographic Details
Published in:Circulation research 2002-08, Vol.91 (3), p.226-231
Main Authors: Regula, Kelly M, Ens, Karen, Kirshenbaum, Lorrie A
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biological and medical sciences
Cell death
Cell Hypoxia
Cells, Cultured
Fundamental and applied biological sciences. Psychology
Heart
Heart Failure - metabolism
Heart Failure - pathology
Heart Ventricles - cytology
Heart Ventricles - metabolism
Intracellular Membranes - metabolism
Ion Channels - metabolism
Membrane Proteins - biosynthesis
Membrane Proteins - genetics
Membrane Proteins - physiology
Mitochondria - metabolism
Mitochondrial Membrane Transport Proteins
Mutation
Permeability
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-bcl-2 - metabolism
Rats
Rats, Sprague-Dawley
Tumor Suppressor Proteins
Vertebrates: cardiovascular system
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Description
Summary:ABSTRACT—In this study, we provide evidence for the operation of BNIP3 as a key regulator of mitochondrial function and cell death of ventricular myocytes during hypoxia. In contrast to normoxic cells, a 5.6-fold increase (P
ISSN:0009-7330
1524-4571
DOI:10.1161/01.RES.0000029232.42227.16