Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (690 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Death, Cell.
Where it fits in the MeSH classification
- Broader topics
- Cell Physiological Phenomena
- Narrower topics
- Cell Death Reversal; Regulated Cell Death
- See also
- Necrosis; Apoptosis
Research landscape
PubMed indexes 439,793 records tagged with the MeSH heading “Cell Death” (counts retrieved 2026-10-29). 124,553 of them (28.3%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 169,771 records.
Reviews account for 42,779 records (9.7%) and meta-analyses for 166. Randomized controlled trials number 662 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 26,647 |
| 2000-2009 | 118,822 |
| 2010-2019 | 169,771 |
| 2020 onward | 124,553 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 42,779 | 9.7% |
| Meta-analyses | 166 | 0.0% |
| Randomized controlled trials | 662 | 0.2% |
Method: PubMed query "Cell Death"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in molecular biology
Molecular biology establishes mechanisms through controlled experiments, often in simplified systems such as purified proteins, cultured cells or model organisms. Such work can show what is possible in a defined system, but whether a pathway matters in a whole organism or in human disease needs further evidence. Check the experimental system, whether findings were reproduced by independent groups, and whether the authors tested the mechanism directly or inferred it from correlation.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Targeted extracellular degradation of LRP8 promotes ferroptosis in cancer cells | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42814555 · DOI · PMC13643147 |
| 4-Hydroxytamoxifen induces a noncanonical ferroptosis in lung adenocarcinoma by targeting AKR1B10 | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42707018 · DOI · PMC13551091 |
| Mesenchymal Stem Cells Alleviate Crohn's Disease by Regulating CBS-Mediated Ferroptosis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42765439 · DOI · PMC13591549 |
Targeted extracellular degradation of LRP8 promotes ferroptosis in cancer cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Tumor reliance on antioxidant defenses creates a vulnerability to ferroptosis, yet strategies to therapeutically disable these systems remain limited.
- Closing excerpt
- More broadly, this work provides a framework for exploiting nutrient acquisition pathways to overcome therapy resistance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (143 words)
Tumor reliance on antioxidant defenses creates a vulnerability to ferroptosis, yet strategies to therapeutically disable these systems remain limited. Here, we identify targeted degradation of the selenium uptake receptor lipoprotein receptor-related protein 8 (LRP8) as an effective approach to decrease the abundance of the ferroptosis-protective enzyme glutathione peroxidase 4 (GPX4). Using bispecific cytokine receptor-targeting chimeras (KineTACs) that couple LRP8 to cytokine receptor internalization pathways, we selectively direct LRP8 to the lysosome for degradation. LRP8 degradation reduces the abundance of several selenoproteins, including GPX4, lowering the cellular threshold for lipid peroxidation and sensitizing cancer cells to ferroptosis. These findings establish receptor-mediated selenium uptake as a critical, targetable node in ferroptosis resistance and demonstrate that extracellular protein degradation can be leveraged to reprogram intracellular translational dependencies in cancer cells. More broadly, this work provides a framework for exploiting nutrient acquisition pathways to overcome therapy resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42814555 · DOI · PMC13643147
4-Hydroxytamoxifen induces a noncanonical ferroptosis in lung adenocarcinoma by targeting AKR1B10 [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundLung adenocarcinoma (LUAD) remains a leading cause of cancer mortality, and current therapies are limited by drug resistance and toxicity.
- Closing excerpt
- AKR1B10 overexpression correlates with poor prognosis and chemoresistance in LUAD.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (302 words)
BackgroundLung adenocarcinoma (LUAD) remains a leading cause of cancer mortality, and current therapies are limited by drug resistance and toxicity. Ferroptosis offers an attractive strategy for cancer therapy, but classical ferroptosis is iron‑dependent. Repurposing approved drugs offers a rapid strategy to identify novel anti‑LUAD agents, yet the mechanism by which 4‑Hydroxytamoxifen (4‑OHT) exerts estrogen receptor-independent anti‑tumour effects remains unclear.MethodsWe performed a drug repurposing screen of 950 endogenous metabolites in LUAD cells. Anti‑tumour activity was validated in vitro and in vivo using LUAD cell lines and mouse models. Target identification and mechanistic studies employed LiP‑MS, pull-down SPR, CETSA, metabolomics, and enzyme activity assays. Clinical relevance was assessed via tissue microarrays and TCGA analysis. Drug synergy was quantified using the Chou-Talalay method.Results4‑OHT inhibited LUAD cell proliferation with IC50 values of 3.86 ± 0.26 µM to 13.58 ± 0.55 µM independent of estrogen receptor. It triggered noncanonical ferroptosis characterised by GSH depletion (reduced by about 60%), GPX4 downregulation, lipid peroxidation (about 2.5-fold increase), and iron independence. Mechanistically, 4‑OHT directly bound AKR1B10 (KD(M) was 7.98e-06) and inhibited its enzymatic activity, leading to ACC1 degradation, lipid deficiency, and accumulation of toxic lipid‑derived carbonyls. AKR1B10 knockout abolished 4‑OHT‑induced cell death, while rescue restored sensitivity. Nanatinostat similarly targeted AKR1B10 and induced the same cell death modality. AKR1B10 upregulation in LUAD tissues correlated with reduced overall survival rates.ConclusionThis study demonstrates that 4‑OHT directly inhibits AKR1B10 enzymatic activity to induce a noncanonical ferroptosis in LUAD. AKR1B10 overexpression correlates with poor prognosis and chemoresistance in LUAD patients. Nonetheless, AKR1B10 inhibition warrants further investigation as a therapeutic strategy.Highlights4‑OHT directly inhibits AKR1B10 enzymatic activity to induce noncanonical ferroptosis in LUAD. AKR1B10 sustains LUAD survival by stabilising ACC1 and detoxifying reactive carbonyl species (RCSs). Nanatinostat similarly targets AKR1B10 and elicits the same cell death modality. AKR1B10 overexpression correlates with poor prognosis and chemoresistance in LUAD.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42707018 · DOI · PMC13551091
Mesenchymal Stem Cells Alleviate Crohn's Disease by Regulating CBS-Mediated Ferroptosis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundMesenchymal stem cells (MSCs) possess immunoregulatory properties and have been shown to alleviate symptoms of Crohn's disease (CD).
- Closing excerpt
- DiscussionThis study demonstrates that MSCs alleviate the symptoms of CD by regulating CBS-mediated ferroptosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
BackgroundMesenchymal stem cells (MSCs) possess immunoregulatory properties and have been shown to alleviate symptoms of Crohn's disease (CD). While ferroptosis has been implicated in the onset of CD, the precise connection between MSCs, CD, and ferroptosis remains unclear. This study sought to explore whether MSCs could alleviate CD by inhibiting ferroptosis.Materials and methodsWe screened the hub genes involved in both ferroptosis and CD and validated them in clinical colon biopsies by immunohistochemistry (IHC). MSCs were administered intraperitoneally to mice with colitis induced by trinitrobenzene sulfonic acid (TNBS) enema to evaluate the therapeutic effect. Additionally, a rescue experiment was conducted by co-treating colitis mice with a cystathionine-β-synthase (CBS) inhibitor (aminooxyacetic acid, AOAA) and MSCs to further explore the mechanism of the MSCs-CBS-ferroptosis axis. The expression levels of CBS and ferroptosis-related markers in colonic tissues were assessed by real-time quantitative polymerase chain reaction (RT-qPCR), western blot, and IHC.ResultsBioinformatics and machine learning identified CBS as a hub gene in both CD and ferroptosis. IHC revealed that CBS expression was downregulated in colon tissues from CD patients. MSCs treatment significantly reduced pathological symptoms and intestinal inflammation in colitis mice. MSCs increased CBS expression, which had been diminished in colitis mice. Additionally, MSCs increased glutathione (GSH) and glutathione peroxidase 4 (GPX4) expression, thereby inhibiting ferroptosis activation. In a rescue experiment, co-treatment with AOAA and MSCs exacerbated intestinal inflammation and reversed the elevation of CBS and ferroptosis-related markers.DiscussionThis study demonstrates that MSCs alleviate the symptoms of CD by regulating CBS-mediated ferroptosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42765439 · DOI · PMC13591549
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Androgen Receptor Variants Confer Castration Resistance in Prostate Cancer by Counteracting Antiandrogen-Induced Ferroptosis [4]
- Research article (99m)Tc-Annexin A5 quantification of apoptotic tumor response: a systematic review and meta-analysis of clinical imaging trials [5]
- Research article Ferroptosis resistance mechanisms in endometriosis for diagnostic model establishment [6]
- Research article Naringenin induces intrinsic and extrinsic apoptotic signaling pathways in cancer cells: A systematic review and meta-analysis of in vitro and in vivo data [7]
- Research article Mesenchymal stem cells-derived small extracellular vesicles and apoptotic extracellular vesicles for wound healing and skin regeneration: a systematic review and meta-analysis of preclinical studies [8]
- Research article Divergent Effects of Arsenic on NF-κB Signaling in Different Cells or Tissues: A Systematic Review and Meta-Analysis [9]
References
- Zhao F, Inague A, Peters-Clarke TM, Chen Y, Ganjave SD, Zhang Y, et al.. Targeted extracellular degradation of LRP8 promotes ferroptosis in cancer cells. . 2026. PMID 42814555 · DOI · PMC13643147
- Yang H, Wang Y, Jin J, Xu H, Miao Y, Wu X, et al.. 4-Hydroxytamoxifen induces a noncanonical ferroptosis in lung adenocarcinoma by targeting AKR1B10. . 2026. PMID 42707018 · DOI · PMC13551091
- Huang Z, Xu X, Huang Z, Han B, Jiang D, Lv X, et al.. Mesenchymal Stem Cells Alleviate Crohn's Disease by Regulating CBS-Mediated Ferroptosis. . 2026. PMID 42765439 · DOI · PMC13591549
- Sun R, Yan B, Li H, Ding D, Wang L, Pang J, et al.. Androgen Receptor Variants Confer Castration Resistance in Prostate Cancer by Counteracting Antiandrogen-Induced Ferroptosis. Cancer Res. 2023. PMID 37527336 · DOI · PMC10543964
- Belhocine TZ, Blankenberg FG, Kartachova MS, Stitt LW, Vanderheyden JL, Hoebers FJ, et al.. (99m)Tc-Annexin A5 quantification of apoptotic tumor response: a systematic review and meta-analysis of clinical imaging trials. Eur J Nucl Med Mol Imaging. 2015. PMID 26275392 · DOI
- Li B, Duan H, Wang S, Li Y. Ferroptosis resistance mechanisms in endometriosis for diagnostic model establishment. Reprod Biomed Online. 2021. PMID 33992553 · DOI
- Faramarzi F, Alimohammadi M, Rahimi A, Alizadeh-Navaei R, Shakib RJ, Rafiei A. Naringenin induces intrinsic and extrinsic apoptotic signaling pathways in cancer cells: A systematic review and meta-analysis of in vitro and in vivo data. Nutr Res. 2022. PMID 35797732 · DOI
- Zhu Y, Yang H, Yang H, Xue Z, Tang H, Chen X, et al.. Mesenchymal stem cells-derived small extracellular vesicles and apoptotic extracellular vesicles for wound healing and skin regeneration: a systematic review and meta-analysis of preclinical studies. J Transl Med. 2025. PMID 40128791 · DOI · PMC11934660
- Wei M, Liu J, Xu M, Rui D, Xu S, Feng G, et al.. Divergent Effects of Arsenic on NF-κB Signaling in Different Cells or Tissues: A Systematic Review and Meta-Analysis. Int J Environ Res Public Health. 2016. PMID 26821040 · DOI · PMC4772183
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.