Abstract
Cell death is a necessary event in multi-cellular organisms to maintain homeostasis by eliminating unrequired or damaged cells. Currently, there are many forms of cell death, and several of them, such as necroptosis, pyroptosis and ferroptosis, even apoptosis trigger an inflammatory response by releasing damage-associated molecular patterns (DAMPs), which are involved in the pathogenesis of a variety of human inflammatory diseases, including autoimmunity disease, diabetes, Alzheimer’s disease and cancer. Therefore, the occurrence of inflammatory cell death must be strictly regulated. Recently, increasing studies suggest that phosphorylation plays a critical role in inflammatory cell death. In this review, we will summarize current knowledge of the regulatory role of phosphorylation in inflammatory cell death and also discuss the promising treatment strategy for inflammatory diseases by targeting related protein kinases that mediate phosphorylation or phosphatases that mediate dephosphorylation.
Highlights
Cell death is a process common to all creatures
Non-programmed cell death (PCD) is referred as accidental cell death (ACD), Which is stimulated by many external factors, such as infection, toxins and physical damage that cause morphological changes, for instance cytoplasmic swelling, rupture of the plasma membrane, and subsequent loss of cell contents, there is no severe chromatin condensation, but with random degradation of DNA [3]
Apoptosis is a process of cell suicide triggered by foreign factor, It’s the spontaneous, orderly death of cells controlled by certain genes, one highly regulated programmed cell death (PCD) [86], The characteristics of apoptosis are cell becoming small and fine cytoplasmic density increased, mitochondrial membrane permeability changed, cytochrome C released into the cytoplasm, the nucleus shrinks, and eventually forms apoptosome, which are engulfed by phagocytes [87, 88]
Summary
Reviewed by: Atsushi Koike, Osaka University of Pharmaceutical Sciences, Japan Shankargouda Patil, Jazan University, Saudi Arabia Divakar Sharma, University of Delhi, India. Cell death is a necessary event in multi-cellular organisms to maintain homeostasis by eliminating unrequired or damaged cells. There are many forms of cell death, and several of them, such as necroptosis, pyroptosis and ferroptosis, even apoptosis trigger an inflammatory response by releasing damage-associated molecular patterns (DAMPs), which are involved in the pathogenesis of a variety of human inflammatory diseases, including autoimmunity disease, diabetes, Alzheimer’s disease and cancer. The occurrence of inflammatory cell death must be strictly regulated. Increasing studies suggest that phosphorylation plays a critical role in inflammatory cell death. We will summarize current knowledge of the regulatory role of phosphorylation in inflammatory cell death and discuss the promising treatment strategy for inflammatory diseases by targeting related protein kinases that mediate phosphorylation or phosphatases that mediate dephosphorylation
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