Cell death, distintos tipos de muerte celular

muerte celular tipos

1. Cell death

2. Terms including intrinsic apoptosis, “apo” (απο) can be taken as “separation” The suffix, “ptosis” (), translated as “falling off Extrinsic apoptosis, mitochondrial permeability transition (MPT)- driven necrosis, necroptosis , ferroptosis , pyroptosis , parthanatos , entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized

3. Accidental cell death (ACD). Virtually instantaneous and uncontrollable form of cell death corresponding to the physical disassembly of the plasma membrane caused by extreme physical, chemical, or mechanical cues. Anoikis . Speci fi c variant of intrinsic apoptosis initiated by the loss of integrin-dependent anchorage. Autophagy-dependent cell death. A form of RCD that mechanistically depends on the autophagic machinery (or components thereof). Autosis . A speci fi c instance of autophagy-dependent cell death that critically relies on the plasma membrane Na - ATPase . Cell death. Irreversible degeneration of vital cellular functions (notably ATP production and preservation of redox homeostasis) culminating in the loss of cellular integrity (permanent plasma membrane permeabilization or cellular fragmentation). Cellular senescence. Irreversible loss of proliferative potential associated with speci fi c morphological and biochemical features, including the senescence-associated secretory phenotype (SASP). Cellular senescence does not constitute a form of RCD. Efferocytosis. Mechanism whereby dead cells and fragments thereof are taken up by phagocytes and disposed. Entotic cell death. A type of RCD that originates from actomyosin-dependent cell-in-cell internalization ( entosis ) and is executed by lysosomes . Extrinsic apoptosis. Speci fi c variant of RCD initiated by perturbations of the extracellular microenvironment detected by plasma membrane receptors, propagated by CASP8 and precipitated by executioner caspases, mainly CASP3. Ferroptosis. A form of RCD initiated by oxidative perturbations of the intracellular microenvironment that is under constitutive control by GPX4 and can be inhibited by iron chelators and lipophilic antioxidants. Immunogenic cell death. A form of RCD that is suf fi cient to activate an adaptive immune response in immunocompetent hosts. Intrinsic apoptosis. Type of RCD initiated by perturbations of the extracellular or intracellular microenvironment, demarcated by MOMP, and precipitated by executioner caspases, mainly CASP3. Lysosome-dependent cell death. A type of RCD demarcated by primary LMP and precipitated by cathepsins, with optional involvement of + + /K MOMP and caspases . Mitochondrial permeability transition (MPT)-driven necrosis. Speci fi c form of RCD triggered by perturbations of the intracellular microenvironment and relying on CYPD. Mitotic catastrophe. Oncosuppressive mechanism for the control of mitosis-incompetent cells by RCD or cellular senescence. Per se, mitotic catastrophe does not constitute a form or RCD. Mitotic death. Speci fi c variant of RCD (most often, intrinsic apoptosis) driven by mitotic catastrophe. Necroptosis. A modality of RCD triggered by perturbations of extracellular or intracellular homeostasis that critically depends on MLKL, RIPK3, and (at least in some settings) on the kinase activity of RIPK1. NETotic cell death. A ROS-dependent modality of RCD restricted to cells of hematopoietic derivation and associated with NET extrusion. Parthanatos . A modality of RCD initiated by PARP1 hyperactivation and precipitated by the consequent bioenergetic catastrophe coupled to AIF- dependent and MIF- dependent DNA degradation . Programmed cell death (PCD). Particular form of RCD that occurs in strictly physiological scenarios, i.e., it does not relate to perturbations of homeostasis and hence does not occur in the context of failing adaptation to stress. Pyroptosis . A type of RCD that critically depends on the formation of plasma membrane pores by members of the gasdermin protein family, often (but not always) as a consequence of in fl ammatory caspase activation. Regulated cell death (RCD). Form of cell death that results from the activation of one or more signal transduction modules, and hence can be pharmacologically or genetically modulated (at least kinetically and to some extent).

4. to) growth factor withdrawal, DNA damage, endoplasmic reticulum (ER) stress, reactive oxygen species (ROS) overload, replication stress, microtubular alterations or mitotic defects [ 29 – 34 ]. Apoptotic cells retain plasma membrane integrity and metabolic activity (to some degree) as the process proceeds to completion, which — in vivo — allows for the rapid clearance by macrophages or other cells with phagocytic activity (a process commonly known as efferocytosis) [ 35 ]. Importantly, intrinsic (and extrinsic, see The critical step for intrinsic apoptosis is irreversible and widespread mitochondrial outer membrane permeabilization (MOMP) which is controlled by pro-apoptotic and anti-apoptotic members of the BCL2, apoptosis regulator (BCL2) protein family In response to apoptotic stimuli, MOMP is mediated by BCL2 associated X, apoptosis regulator (BAX), and/ or BCL2 antagonist / killer 1 (BAK1; best known as BAK) BAX and BAK are the only BCL2 family members characterized so far in mammalian cells for their ability to form pores across the outer mitochondrial membrane (OMM) and possibly other intracellular membranes BID, BIM, PUMA, and NOXA share the ability to physically (but transiently) interact with the mitochondrial pool of BAX and/or BAK (hence being known as “ activators ” ) to promote a series of conformational changes

5. BCL2 representing the pharmacological target of the FDA-approved BH3 mimetic venetoclax (also known as ABT-199) and other molecules with a similar mechanism canonical BAX and BAK activation remains to be formally established. Both anti-apoptotic and pro-apoptotic BCL2 proteins are also subjected to tight transcriptional and post-translational regulation, involving (but not limited to) proteasomal degradation, phosphorylation, and subcellular (re)localization [ 48 , 108 , 133 – 138 ]. Finally, it is becoming increasingly evident that mitochondrial size and shape [ 139 – 141 ] as well as lipid composition [ 142 , 143 ] can

6. MOMP directly promotes the cytosolic release of apoptogenic factors that normally reside in the mitochondrial intermembrane space [ 40 , 44 , 156 ]. These mitochondrial proteins include (but are not limited to) cytochrome c, somatic (CYCS), which usually operates as an electron shuttle in the mitochondrial respiratory chain [ 157 – 160 ],