Molecular Mechanisms of Apoptosis in Disease Pathogenesis and Targets for Therapeutic Intervention

Dear Colleagues,

The last several decades have revealed and characterized, in ever greater detail, a set of genetically encoded regulators for the targeted elimination of surplus, irreversibly damaged, and potentially destructive cells. Novel molecular pathways of cell death continue to be discovered, and now include intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, NETotic cell death, autophagy-dependent cell death, and mitotic catastrophe. Apoptosis is a physiological form of programmed cell death (PCD) characterized by cell shrinkage, chromatin condensation (pyknosis), nuclear fragmentation (karyorrhexis), loss of mitochondrial membrane potential, caspase activation, and plasma membrane blebbing, culminating with the formation of apoptotic bodies that are phagocytosed by neighboring cells or macrophages and degraded within lysosomes. 

In this Special Issue of Cells, we invite you to contribute original research articles or reviews that focus on the roles of specific genes, molecular mechanisms, signaling cascades, and regulators of apoptosis, which are important in both normal development, tissue homeostasis, and the etiology of an increasing number of pathophysiological conditions. Abnormalities in apoptotic regulation have been shown to play a critical role in the pathogenesis of these diseases, and delineating the roles of specific genes and targeting these genes involved holds promise for effective treatment. This Special Issue will highlight the practical aspects of modulating this process in the development of therapeutic approaches to cancer, myocardial infarction, ischemic disorders, spinal cord injuries, bacterial and viral infection, as well as autoimmune and neurodegenerative diseases. More efficient therapeutic strategies are being developed to generate apoptosis modulators for clinical use that can potentially target these molecular machineries by genetic or pharmacological intervention.

We look forward to receiving your contributions.

Dr. Cynthia Simbulan-Rosenthal
Dr. Dean S. Rosenthal
Guest Editors

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• apoptosis
• programmed cell death
• caspases
• Bcl2 family
• cancer
• neurodegenerative diseases
• myocardial infarction
• viral infection
• intrinsic apoptosis
• extrinsic apoptosis
• mitochondrial permeability transition