Physiologic and pathophysiologic role of calpain: implications for the occurrence of atrial fibrillation.

Abstract

Calpain is an intracellular Ca(2+)-activated protease and an important mediator of the actions of calcium. Cleavage by calpain is critical in a variety of calcium-regulated cellular processes such as muscle contraction, neuronal excitability, secretion, signal transduction, cell proliferation, differentiation, cell cycle progression, and apoptosis. Deregulation of calpain caused by a disruption of calcium homeostasis during cardiac pathologies such as atrial fibrillation, heart failure, hypertrophy, or ischemia reperfusion, is critically involved in the myocardial damage. This review will summarize the physiologic and pathophysiologic basis of calpain. Atrial fibrillation is chosen as one example to explain the specific consequences of an increased calpain activity in cardiac muscle.

• Authors: Alicja Bukowska, Uwe Lendeckel, Stefanie M Bode-Böger, Andreas Goette
• Journal: Cardiovascular therapeutics (Cardiovasc Ther) Vol. 30 Issue 3 Pg. e115-27 (Jun 2012) ISSN: 1755-5922 [Electronic] England
• PMID: 21108772 (Publication Type: Journal Article, Review)
• Copyright: © 2010 Blackwell Publishing Ltd.

Chemical References

• Cardiovascular Agents
• Cysteine Proteinase Inhibitors
• Fibrinolytic Agents
• Calpain

Topics

• Animals
• Atrial Fibrillation (drug therapy, enzymology, etiology, physiopathology)
• Calpain (antagonists & inhibitors, metabolism)
• Cardiovascular Agents (therapeutic use)
• Cysteine Proteinase Inhibitors (therapeutic use)
• Enzyme Activation
• Fibrinolytic Agents (therapeutic use)
• Heart Atria (enzymology, physiopathology)
• Humans
• Myocardium (enzymology)
• Risk Assessment
• Risk Factors