Abstract
Apoptosis has been causally linked to the pathogenesis of myocardial infarction and heart failure in rodent models. This death process is mediated by two central pathways, an extrinsic pathway involving cell surface receptors and an intrinsic pathway using mitochondria and the endoplasmic reticulum. Each of these pathways has been implicated in myocardial pathology. In this review, we summarize recent advances in the understanding of the intrinsic pathway and how it relates to cardiac myocyte death and heart disease.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
-
Review
MeSH terms
-
Animals
-
Apoptosis / physiology*
-
Apoptosis Inducing Factor
-
Caspases / physiology
-
Cytochromes c / metabolism
-
Endoplasmic Reticulum / physiology
-
Enzyme Activation
-
Flavoproteins / pharmacology
-
Gene Expression Regulation
-
Heart Diseases / pathology
-
Humans
-
Ion Channels / physiology
-
Membrane Proteins / pharmacology
-
Mitochondria, Heart / physiology*
-
Mitochondrial Membrane Transport Proteins
-
Mitochondrial Permeability Transition Pore
-
Myocytes, Cardiac / cytology*
-
Protein Structure, Tertiary
-
Proto-Oncogene Proteins / chemistry
-
Proto-Oncogene Proteins / physiology
-
Rodentia
-
Stress, Physiological / pathology
-
Tumor Suppressor Protein p53 / physiology
Substances
-
AIFM1 protein, human
-
Apoptosis Inducing Factor
-
Flavoproteins
-
Ion Channels
-
Membrane Proteins
-
Mitochondrial Membrane Transport Proteins
-
Mitochondrial Permeability Transition Pore
-
Proto-Oncogene Proteins
-
Tumor Suppressor Protein p53
-
Cytochromes c
-
Caspases