In the normal process of ageing, cell death occurs by an 'intrinsic' programmed gene-mediated sequence of cell shrinkage and nuclear condensation called apoptosis. However, apoptosis may be accelerated by the extrinsic pathological processes described above which result in cell injury and swelling. Apoptosis and extrinsic cell injury have several mechanisms in common, including changes in gene expression and calcium influx, again suggesting the possibility of a link between constitutional susceptibility and acquired disease. Whatever the process, removal of necrotic cell debris by phagocytosis will be impaired if the volume of dead tissue is large or if phagocytic capacity is impaired by immunoincompetence induced by drugs or nutritional depletion. Under these circumstances, tissue remodeling will be delayed with prolongation of organ failures.
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