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Apoptotic cell death in disease—Current understanding of the NCCD 2023

Authors: Vitale, Ilio; Pietrocola, Federico; Guilbaud, Emma; Aaronson, Stuart A.; Abrams, John M.; Adam, Dieter; Agostini, Massimiliano; +193 Authors

Apoptotic cell death in disease—Current understanding of the NCCD 2023

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Countries
Germany, United States, Belgium, Italy, Germany, Netherlands, United Kingdom, Poland, Denmark, Belgium, United Kingdom, Italy, United Kingdom, Italy, Germany, Australia, United Kingdom, Italy, United Kingdom, France, Italy, Italy, Italy, United Kingdom, Australia, France, Denmark, Italy, Argentina, Italy, Italy
Keywords

Settore BIOS-09/A - Biochimica clinica e biologia molecolare clinica, Biomedical and clinical sciences, Physiology, Carcinogenesis, NF-KAPPA-B, ISCHEMIA-REPERFUSION INJURY, Apoptosis, Pathogenesis, Review Article, Medical and Health Sciences, Settore MEDS-06/A - Chirurgia generale, FAS-LIGAND GENE, Settore BIO/12 - BIOCHIMICA CLINICA E BIOLOGIA MOLECOLARE CLINICA, Apoptosis/genetics, https://purl.org/becyt/ford/3.1, 2.1 Biological and endogenous factors, /dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being; name=SDG 3 - Good Health and Well-being, 11 Medical and Health Sciences, TUMOR-NECROSIS-FACTOR, Mammals, Settore BIO/11 - BIOLOGIA MOLECOLARE, /dk/atira/pure/subjectarea/asjc/1300/1312; name=Molecular Biology, genetics [Caspases], Mammals/metabolism, Cell Death, apoptosis, metabolism [Mammals], Settore BIOS-08/A - Biologia molecolare, Biological Sciences, genetic strategies, APOPTOSIS, [SDV] Life Sciences [q-bio], Biological sciences, Chemistry, regulated cell death (RCD), cell death, EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS, DISEASES, cell loss and tissue damage, Caspases, THERAPEUTICS, Life Sciences & Biomedicine, BH3-ONLY PROTEIN BIM, 570, Biochemistry & Molecular Biology, Caspases/genetics, 1.1 Normal biological development and functioning, 610, TRAUMATIC BRAIN-INJURY, CELL DEATH, cell death; disease, caspases, Medical research, apoptosis; cell death, cancer, BCL-2 FAMILY-MEMBER, metabolism [Caspases], Animals, Humans, https://purl.org/becyt/ford/3, TRANSGENIC MOUSE MODEL, Settore BIO/10 - BIOCHIMICA, Biology, genetics [Apoptosis], Science & Technology, 42 Health sciences, Cell death, diseases, 31 Biological sciences, Health sciences, Cell Biology, 32 Biomedical and clinical sciences, 06 Biological Sciences, apoptosi, Settore MED/18, /dk/atira/pure/subjectarea/asjc/1300/1307; name=Cell Biology, Good Health and Well Being, n/a, Biochemistry and Cell Biology, Generic health relevance, Human medicine, FLICE-INHIBITORY PROTEIN, Animals; Apoptosis; Carcinogenesis; Caspases; Cell Death; Humans; Mammals, ddc: ddc:610

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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