Cell Death

Types of cell death are various, including ferroptosis, cuproptosis, necrosis, apoptosis, autophagy etc with different morphological characteristics and molecular mechanisms. Understanding various processes of cell death is very important for learning diseases and developing new therapies.

Necrosis is the external stimuli-induced and uncontrollable cell death. Features include cell swelling, broken membrane and release of cellular contents. Apoptosis is the gene regulated-programmed cell death, showing cell contraction, chromatin condensation, membrane bleeding, nuclear division and formation of apoptosome. Apoptosis-formed cells are divided into small membrane apoptosomes. These apoptosomes can be phagocytized and removed by surrounding cells(e.g. macrophage). Contents released by necrotic cells can activate immune response, cause inflammation and may damage adjacent cells.

Autophagic cell death(type II programmed cell death) is caused by abnormal activation of autophagy pathway. Autophagy is the process during which cells isolate and degrade cytoplasmic components via phagocytic vacuoles. In normal situation, it helps to maintain homeostasis and remove toxic substances. Stimulation of nutritional deficiency, oxidative stress or cytotoxicity can cause cell death induced by autophagy disorder. Induction of autophagy depends on ULK1 complex and is regulated by mTOR pathway. During autophagy, cytoplasm components are enveloped and degraded, possibly resulting in autophagic cell death which promotes or inhibit tumor growth.

Pyroptosis is the soluble and inflammatory programmed cell death, which is usually induced by inflammasome and conducted by gasdermin protein. Main features of pyroptosis are cell swelling, membrane perforation and release of cellular contents. Mechanisms include (non-)classical pathway. In classical pathway, inflammasomes like NLRP3 etc activate Caspase-1. Caspase-1 cleaves GSDMD to form active N-terminal, resulting in the membrane perforation and death by promoting the release of IL-1β and improving inflammatory response. In non-classical pathway, LPS directly activates Caspase-4/5/11, and cleaves GSDMD, resulting in pyroptosis via N-terminal and active Pannexin-1 pathway. Release of ATP and K+ active NLRP3 inflammasomes, finally promoting release of IL-1β and cell death.

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