The two principal types of programmed cell death are apoptosis and autophagy-associated cell death. The recognition that cell death can occur by genetically controlled processes has aided advances in unveiling the mechanisms of many diseases. As a result, we now have improved knowledge of the initiation of cell death programs and the relevant signaling pathways. This information has facilitated development of pharmacologic agents that initiate or inhibit programmed cell death. Moreover, there is now evidence that necrosis, traditionally considered an accidental form of cell death, can, in certain instances, be initiated or modulated under programmed control mechanisms.
Mounting evidence in the context of cell death pathways has led to development of promising novel therapies. Despite these advances, answers to a number of enigmatic and interesting questions remain. Why some cell types are much more vulnerable to ischemic cell death than most others? How does a cell select a particular type of death and execute? How does a cell switch from a stress or environmental insults recovery program to cell death? What criteria propel the alternative of cell death pathway? When is a cell committed to death? Such understandings will make us land in a profound understanding of cell death, an expanding foundation on which increasingly effective therapeutic interventions may be modeled and introduced into clinical practice in diverse diseases. The current special issue will address multi factorial approaches in the area of cell death pathways in multiple diseases.
Dr. Rohit Gundamaraju and Dr. Niraj Kumar Jha
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