Key result
Ischaemic necrosis in the myocardium causes loss of cell membrane integrity, leakage of intracellular proteins, cellular swelling, and an acute inflammatory response followed by fibrosis.
Provides a descriptive overview of the cellular and molecular processes involved in ischaemic necrosis and apoptosis in the myocardium.
Explains troponin release and post-MI remodeling; confirms established mechanisms while leaving open targeted anti-inflammatory strategies.
Cardiologists are well acquainted with cell death due to ischaemic necrosis in the myocardium. Loss of the integrity of the cell membrane leads to leakage of intracellular dehydrogenases and kinases, as well as struc- tural proteins such as troponin T, into the interstitial spaces and ultimately into the plasma. Fluid and ions flood into the cell caus- ing the cytoplasmic swelling which is observed by microscopy in early necrosis. Mitochondrial swelling and disruption occur early in necrosis while nuclear fragmentation occurs late in the process. The necrotic cells invoke an acute inflammatory response and complement is bound; repair by fibrosis follows.
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Michael J. Davies (1997) conducted a review in Cardiovascular disease. Ischaemic necrosis in the myocardium causes loss of cell membrane integrity, leakage of intracellular proteins, cellular swelling, and an acute inflammatory response followed by fibrosis.
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