"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 | ApoptosisApoptosisProgrammed Cell Death, Type I
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				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 | 
|---|
| 1995 | 2 | 4 | 6 | 
| 1996 | 5 | 2 | 7 | 
| 1997 | 16 | 8 | 24 | 
| 1998 | 22 | 11 | 33 | 
| 1999 | 14 | 9 | 23 | 
| 2000 | 15 | 18 | 33 | 
| 2001 | 13 | 22 | 35 | 
| 2002 | 22 | 24 | 46 | 
| 2003 | 19 | 24 | 43 | 
| 2004 | 22 | 41 | 63 | 
| 2005 | 31 | 27 | 58 | 
| 2006 | 24 | 32 | 56 | 
| 2007 | 23 | 31 | 54 | 
| 2008 | 18 | 34 | 52 | 
| 2009 | 18 | 45 | 63 | 
| 2010 | 18 | 41 | 59 | 
| 2011 | 23 | 52 | 75 | 
| 2012 | 14 | 33 | 47 | 
| 2013 | 12 | 51 | 63 | 
| 2014 | 18 | 60 | 78 | 
| 2015 | 23 | 52 | 75 | 
| 2016 | 12 | 47 | 59 | 
| 2017 | 18 | 50 | 68 | 
| 2018 | 15 | 30 | 45 | 
| 2019 | 5 | 43 | 48 | 
| 2020 | 11 | 45 | 56 | 
| 2021 | 4 | 42 | 46 | 
| 2022 | 3 | 14 | 17 | 
| 2023 | 2 | 16 | 18 | 
| 2024 | 15 | 17 | 32 | 
| 2025 | 2 | 10 | 12 | 
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				Below are the most recent publications written about "Apoptosis" by people in Profiles.
						
					
								- 
								CYP1B1 Mediates Cigarette Smoke-Induced Lipid Accumulation in Alveolar Type 2 Cells. FASEB J. 2025 Sep 30; 39(18):e71062. 
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								Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging. Nat Commun. 2025 Aug 25; 16(1):7591. 
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								Developmental Endothelial Locus 1 Reduces Traumatic Brain Injury-Induced Endotheliopathy and Dysregulated Coagulation in Mice. Arterioscler Thromb Vasc Biol. 2025 Sep; 45(9):e454-e466. 
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								Polo-like kinase 1 inactivation enhances PI3K inhibition-mediated apoptosis of NOTCH1-mutant head and neck squamous cell carcinoma. Cancer Lett. 2025 Aug 10; 625:217814. 
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								Glioblastoma-instructed astrocytes suppress tumour-specific T cell immunity. Nature. 2025 Jul; 643(8070):219-229. 
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								G-quadruplex stabilizer CX-5461 effectively combines with radiotherapy to target a-thalassemia/mental retardation X-linked-deficient malignant glioma. Neuro Oncol. 2025 May 15; 27(4):932-947. 
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								TFEB Orchestrates Stress Recovery and Paves the Way for Senescence Induction in Human Dermal Fibroblasts. Aging Cell. 2025 Jul; 24(7):e70083. 
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								Screening and identification of versican as a sensitive biomarker and potential therapeutic target in basal cell carcinoma. Int J Med Sci. 2025; 22(10):2488-2501. 
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								Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and apoptotic pathways. J Pharm Sci. 2025 Jul; 114(7):103802. 
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								PARP inhibitor response is enhanced in prostate cancer when XRCC1 expression is reduced. NAR Cancer. 2025 Jun; 7(2):zcaf015.