Programmed cell death (PCD) is, in contrast to non-programmed cell death (or necrosis), controlled by active signaling pathways that translate external stimuli in cellular responses. PCD occurs during normal organismal development and underlies tissue homeostasis and organ function. Genetic defects or aqcuired resistance against certain forms of PCD are linked to a wide spectrum of pathophysiological conditions, like tumor formation, inflammatory responses and infection diseases.
Apart from autophagy-induced cell death and caspase-dependent apoptosis, caspase-independent PCDs, like pyroptosis, parthanatos, ferroptosis and necroptosis, are programmed forms of necrosis. Besides PCD-specific molecular and cellular signaling mechanisms, PCDs affect the functional outcome by directly influencing the immunological answer, ranging from non/less immunogenic forms of PCD, like apoptosis, to highly inflammatory responses observed by necroptosis or ferroptosis.
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