ReviewBiomedical journal2023
Cellular senescence and the host immune system in aging and age-related disorders.
Review in Biomedical journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Immunological consequences of senescence in physiology and pathology.Journal of translational medicine · 2026Review
- Displaced minds: ecologies of depression.Biomedical journal · 2026Article
- A machine learning-driven framework integrating cell death and senescence signatures for multi-target drug design and immunotherapy optimization in ovarian cancer.NPJ precision oncology · 2026Article
- Risk factors and prediction model for acute respiratory distress syndrome in patients with digestive tumor after surgery.World journal of gastrointestinal surgery · 2026Article
- Immunosuppressive macrophages determine the effect of cellular senescence on tumor progression.Science advances · 2026Article
- Cellular senescence and metabolic aging in type 2 diabetes: mechanistic insights and translational implications.Frontiers in endocrinology · 2026Review
- Therapy-induced senescence in breast cancer and cardiovascular disease: a double-edged biological process.Frontiers in cardiovascular medicine · 2026Review
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Cellular senescence in cancer immunology and potential therapeutic strategy.Frontiers in oncology · 2026Review
- Comprehensive characterisation of age-related changes in cell subpopulations and tissue structural properties in secondary lymphoid organs.Cell death & disease · 2025Article
- Reprogramming cellular senescence and aging clocks for advanced cancer immunotherapy.Molecular cancer · 2025Review
- CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging.Nature aging · 2025Article
- Chimeric Antigen Receptor Cell Therapy: Current Status and Its Potential in Aging and Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Lysosome-dependent cell death: disease implications and potential therapeutic targets.Molecular biology reports · 2025Review
- Connections Between Cellular Senescence and Alzheimer's Disease-A Narrative Review.International journal of molecular sciences · 2025Review
- Neurotoxicants driving glial aging: role of astrocytic aging in non-cell autonomous neurodegeneration.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Persistent accumulation of therapy-induced senescent cells: an obstacle to long-term cancer treatment efficacy.International journal of oral science · 2025Review
- Reprogramming cellular senescence of hepatic stellate cells to combat liver fibrosis by targeted nanodrugs.Materials today. Bio · 2025Article
- Role of age in mediating the association between the vaginal microbiota and preterm birth.mSystems · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a complex process involving a close-to-irreversible arrest of the cell cycle, the acquisition of the senescence-associated secretory phenotype (SASP), as well as profound changes in the expression of cell surface proteins that determine the recognition of senescent cells by innate and cognate immune effectors including macrophages, NK, NKT and T cells. It is important to note that senescence can occur in a transient fashion to improve the homeostatic response of tissues to stress. Moreover, both the excessive generation and the insufficient elimination of senescent cells may contribute to pathological aging. Attempts are being made to identify the mechanisms through which senescent cell avoid their destruction by immune effectors. Such mechanisms involve the cell surface expression of immunosuppressive molecules including PD-L1 and PD-L2 to ligate PD-1 on T cells, as well as tolerogenic MHC class-I variants. In addition, senescent cells can secrete factors that attract immunosuppressive and pro-inflammatory cells into the microenvironment. Each of these immune evasion mechanism offers a target for therapeutic intervention, e.g., by blocking the interaction between PD-1 and PD-L1 or PD-L2, upregulating immunogenic MHC class-I molecules and eliminating immunosuppressive cell types. In addition, senescent cells differ in their antigenic makeup and immunopeptidome from their normal counterparts, hence offering the opportunity to stimulate immune response against senescence-associated antigens. Ideally, immunological anti-senescence strategies should succeed in selectively eliminating pathogenic senescent cells but spare homeostatic senescence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.