"Apoptosis" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
| Descriptor ID |
D017209
|
| MeSH Number(s) |
G04.146.160
|
| Concept/Terms |
Apoptosis- Apoptosis
- Programmed Cell Death, Type I
|
Below are MeSH descriptors whose meaning is more general than "Apoptosis".
Below are MeSH descriptors whose meaning is more specific than "Apoptosis".
This graph shows the total number of publications written about "Apoptosis" by people in this website by year, and whether "Apoptosis" was a major or minor topic of these publications.
To see the data from this visualization as text,
click here.
| Year | Major Topic | Minor Topic | Total |
|---|
| 1999 | 3 | 0 | 3 |
| 2000 | 0 | 1 | 1 |
| 2001 | 2 | 0 | 2 |
| 2002 | 2 | 1 | 3 |
| 2003 | 1 | 2 | 3 |
| 2004 | 1 | 1 | 2 |
| 2005 | 0 | 5 | 5 |
| 2006 | 0 | 1 | 1 |
| 2007 | 1 | 3 | 4 |
| 2009 | 1 | 2 | 3 |
| 2010 | 0 | 1 | 1 |
| 2011 | 1 | 1 | 2 |
| 2012 | 0 | 1 | 1 |
| 2015 | 0 | 2 | 2 |
| 2016 | 0 | 1 | 1 |
| 2017 | 0 | 3 | 3 |
| 2018 | 0 | 1 | 1 |
| 2022 | 0 | 1 | 1 |
| 2025 | 0 | 1 | 1 |
| 2026 | 0 | 1 | 1 |
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Below are the most recent publications written about "Apoptosis" by people in Profiles.
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Endothelial c-IAP2 loss amplifies P2X7 receptor-driven inflammation and worsens schistosomiasis-associated pulmonary hypertension. Proc Natl Acad Sci U S A. 2026 06 23; 123(25):e2513158123.
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Unravelling the anti-cancer mechanisms elicited by non-covalent thioredoxin reductase inhibitors for triple negative breast cancer therapy. Redox Biol. 2026 03; 90:103980.
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Presence of CrkI-containing microvesicles in squamous cell carcinomas could have ramifications on tumor biology and cancer therapeutics. Sci Rep. 2022 03 21; 12(1):4803.
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Alpha ketoglutarate levels, regulated by p53 and OGDH, determine autophagy and cell fate/apoptosis in response to Nutlin-3a. Cancer Biol Ther. 2019; 20(3):252-260.
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Ex Vivo Cardiotoxicity of Antineoplastic Casiopeinas Is Mediated through Energetic Dysfunction and Triggered Mitochondrial-Dependent Apoptosis. Oxid Med Cell Longev. 2018; 2018:8949450.
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Selective neutralization of IL-12 p40 monomer induces death in prostate cancer cells via IL-12-IFN-?. Proc Natl Acad Sci U S A. 2017 10 24; 114(43):11482-11487.
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The IGF-1R/AKT pathway has opposing effects on Nutlin-3a-induced apoptosis. Cancer Biol Ther. 2017 Nov 02; 18(11):895-903.
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The effects of blood and blood products on the arachnoid cell. Exp Brain Res. 2017 06; 235(6):1749-1758.
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Small Interfering RNA Targeting Mitochondrial Calcium Uniporter Improves Cardiomyocyte Cell Viability in Hypoxia/Reoxygenation Injury by Reducing Calcium Overload. Oxid Med Cell Longev. 2017; 2017:5750897.
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The influence of fibroblast on the arachnoid leptomeningeal cells in vitro. Brain Res. 2017 02 15; 1657:109-119.