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Cardiac surgical implications of calcium dyshomeostasis in the heart
D R Meldrum1, J C Cleveland, B C Sheridan
1Department of Surgery, University of Colorado Health Sciences Center, Denver 80262, USA.
Insights
Myocardial ischemia, a major cause of death, can be treated by cardiac preconditioning. This transient protective state, involving calcium (Ca2+) regulation, offers therapeutic potential against surgical ischemic events.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Coronary artery disease leads to myocardial ischemia, a significant cause of mortality.
- Cardiac surgery can induce myocardial ischemia and reperfusion injury.
- Intracellular calcium (Ca2+) regulation is crucial for myocyte function and cardiac health.
Purpose of the Study:
- To explore the role of intracellular calcium regulation in myocardial ischemia.
- To investigate the therapeutic potential of cardiac preconditioning against ischemia-reperfusion injury.
- To examine the link between Ca2+ transport gene expression and myocardial dysfunction.
Main Methods:
- Review of existing literature on calcium transport and myocardial function.
- Analysis of signaling pathways involving protein kinase C and Ca2+.
- Examination of therapeutic strategies targeting intracellular calcium.
Main Results:
- Altered Ca2+ transport protein gene expression contributes to myocardial dysfunction.
- Protein kinase C and Ca2+ show potential therapeutic roles in protecting the heart.
- Cardiac preconditioning, a transient protective state, can mitigate ischemic events.
Conclusions:
- Intracellular calcium regulation is a key therapeutic target for myocardial ischemia.
- Cardiac preconditioning offers a promising strategy to protect the heart during surgery.
- Further research into Ca2+ signaling pathways could yield novel treatments for cardiac disease.
Abstract:
The prevalence of coronary artery disease renders myocardial ischemia a leading cause of morbidity and mortality. Both cardiac bypass operations and cardiac transplantation cause myocardial ischemia and reperfusion injury. Intracellular calcium transport and regulation are of paramount importance in both normal and pathologic myocardial states. Calcium regulation is integral to nearly every myocyte function, from early development to senescence. Normal intracellular calcium-mediated excitation-contraction coupling and abnormal patterns of calcium regulation leading to systolic/diastolic dysfunction are now therapeutically accessible to the cardiac surgeon. Additionally, altered Ca2+ transport protein gene expression is a mechanism of myocardial dysfunction. Therapeutic strategies involve receptor-mediated transduction of signals to intracellular metabolic sites. Evidence implicates protein kinase C as well as a potential therapeutic role for Ca2+. The potential for pharmacologic access to this protective state has abundant clinical appeal. The protective state (cardiac "preconditioning") is transient but is amenable as therapy against operation-related ischemic events.