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[Calpains and cardiac diseases]
C Perrin1, C Vergely, L Rochette
1Laboratoire de physiopathologie et pharmacologie cardiovasculaires expérimentales (LPPCE), IFR N 100, Faculté de médecine, 7, boulevard Jeanne-d'Arc, BP 87900, 21079 Dijon, France. caroline.perrin@u-bourgogne.fr
Annales De Cardiologie Et D'Angeiologie
|November 10, 2004
Summary
Calpain activation, linked to increased cytosolic calcium, contributes to myocardial damage in cardiac pathologies like heart failure and ischemia reperfusion. These proteases degrade key cardiac proteins, promoting cell death.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiology
Context:
- Calpains are cytosolic cysteine proteases with diverse isoforms.
- Ubiquitous calpains (micro- and milli-calpain) are activated by calcium and phospholipids.
- They cleave various substrates, including structural and signaling proteins.
Purpose:
- To explore the role of calpains in cardiac pathologies.
- To investigate calpain involvement in myocardial damage and cell death.
Summary:
- Calpain activation is implicated in cardiac conditions such as heart failure, atrial fibrillation, and ischemia reperfusion injury.
- Elevated calpain activity in affected hearts leads to proteolysis of myocardial components, notably troponins.
- Calpains are involved in mediating myocardial cell death through necrosis and apoptosis.
Impact:
- Understanding calpain's role provides insights into mechanisms of cardiac damage.
- This knowledge may inform therapeutic strategies targeting calpain activity in cardiovascular diseases.