Medical College of Wisconsin
CTSICores SearchResearch InformaticsREDCap

Stress (heat shock) proteins: molecular chaperones in cardiovascular biology and disease. Circ Res 1998 Jul 27;83(2):117-32

Date

08/01/1998

Pubmed ID

9686751

DOI

10.1161/01.res.83.2.117

Scopus ID

2-s2.0-0032572603 (requires institutional sign-in at Scopus site)   813 Citations

Abstract

How a cell responds to stress is a central problem in cardiovascular biology. Diverse physiological stresses (eg, heat, hemodynamics, mutant proteins, and oxidative injury) produce multiple changes in a cell that ultimately affect protein structures and function. Cells from different phyla initiate a cascade of events that engage essential proteins, the molecular chaperones, in decisions to repair or degrade damaged proteins as a defense strategy to ensure survival. Accumulative evidence indicates that molecular chaperones such as the heat shock family of stress proteins (HSPs) actively participate in an array of cellular processes, including cytoprotection. The versatility of the ubiquitous HSP family is further enhanced by stress-inducible regulatory networks, both at the transcriptional and posttranscriptional levels. In the present review, we discuss the regulation and function of HSP chaperones and their clinical significance in conditions such as cardiac hypertrophy, vascular wall injury, cardiac surgery, ischemic preconditioning, aging, and, conceivably, mutations in genes encoding contractile proteins and ion channels.

Author List

Benjamin IJ, McMillan DR

Author

Ivor J. Benjamin MD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Adaptation, Physiological
Animals
Apoptosis
Autoantibodies
Autoimmune Diseases
Cardiovascular Diseases
Cell Nucleus
Chagas Disease
Cytosol
Gene Expression Regulation
Heat-Shock Proteins
Humans
Ion Channels
Ischemic Preconditioning
Models, Biological
Molecular Chaperones
Muscle Development
Muscle Proteins
Muscles
Myocardial Ischemia
Myocardial Reperfusion Injury
Myocardium
Nuclear Proteins
Oxidation-Reduction
Protein Folding
Rabbits
Reactive Oxygen Species