Cells may die by active mechanisms (cellular suicide). The concept of active cell death goes back to the 19th and early 20th century [1]. Active or programmed cell death serves to eliminate excessive cells, e.g. from hyperplastic organs, or cells damaged by moderate injury. Morphologically and biochemically, mechanisms of active cell death may be diVerent in diVerent organs and in different physiological states. Apoptosis (type I) is characterized by cytoplasmic and nuclear condensation, fragmentation, and heterophagy [2]; in type II cell death autophagic/lysosomal processes are prominent which produce cytoplasmic degradation well before nuclear alterations [3, 4].
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Schulte‐Hermann et al. (1998) studied this question.
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