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Apoptosis is a mechanism of programmed cell death and is essential for development and homeostasis. Cell stress stimulates pro-apoptotic signalling pathways that activate caspase proteases and cause mitochondrial dysfunction. Apoptotic cells undergo characteristic changes in cell morphology, including cell rounding, plasma membrane blebbing and nuclear fragmentation.
SmgGDS insufficiency exacerbates the process of cisplatin-induced acute kidney injury through PERK-dependent ER stress, leading to mitochondrial dysfunction and cell death, and overexpression of smgGDS reverses this effect.
Rauh et al. developed a selective MCL1 inhibitor that is efficacious in hematological and solid tumors and has the advantage of limited cardiotoxicity because of more rapid clearance of the drug in vivo.
The spatiotemporal activation of phagocytosis by hair follicle cells is orchestrated by lipids released from surrounding apoptotic cells and retinoids released by healthy cells.
