ReviewBMB reports2015
From cell senescence to age-related diseases: differential mechanisms of action of senescence-associated secretory phenotypes.
Review in BMB reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 64 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
64 citing papers in PubMed, 110 citations in OpenAlex.
- Trial
- Plasma proteomic profiles of lung volume-based phenotypes in tobacco-exposed individuals without spirometric chronic obstructive pulmonary disease.Annals of the American Thoracic Society · 2026Observational
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Exercise-induced changes in circulatory aging-related biomarkers among older adults: longitudinal analysis of a multi-stage randomized clinical trial.Immunity & ageing : I & A · 2026Article
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- Article
- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
- Depletion of senescent cells improves surgery-induced neuroinflammation in aged mice.PNAS nexus · 2025Article
- Targeting Senescence, Oxidative Stress, and Inflammation: Quercetin-Based Strategies for Ocular Diseases in Older Adults.Clinical interventions in aging · 2025Review
- The prognostic implications and oncogenic role of NSUN5 in clear cell renal cell carcinoma.Clinical and experimental medicine · 2024Article
- Oxidized Low-Density Lipoprotein and Its Role in Immunometabolism.International journal of molecular sciences · 2024Review
- Aging aggravates aortic aneurysm and dissection via miR-1204-MYLK signaling axis in mice.Nature communications · 2024Article
- Adoptive NK cell therapy: a potential revolutionary approach in longevity therapeutics.Immunity & ageing : I & A · 2024Review
- Narrative Review of Immunomodulatory and Anti-inflammatory Effects of Sodium-Glucose Cotransporter 2 Inhibitors: Unveiling Novel Therapeutic Frontiers.Kidney international reports · 2024Review
- Nervonic Acid Inhibits Replicative Senescence of Human Wharton's Jelly-Derived Mesenchymal Stem Cells.International journal of stem cells · 2024Article
- Antiaging Strategies and Remedies: A Landscape of Research Progress and Promise.ACS chemical neuroscience · 2024Review
- Modulation of fracture healing by senescence-associated secretory phenotype (SASP): a narrative review of the current literature.European journal of medical research · 2024Review
- Accumulation of senescent cells in the stroma of aged mouse ovary.The Journal of reproduction and development · 2023Article
- Oxymatrine Improves Oxidative Stress-Induced Senescence in HT22 Cells and Mice via the Activation of AMP-Activated Protein Kinase.Antioxidants (Basel, Switzerland) · 2023Article
- Anti-Aging Potential of Platelet Rich Plasma (PRP): Evidence from Osteoarthritis (OA) and Applications in Senescence and Inflammaging.Bioengineering (Basel, Switzerland) · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a process by which cells enter a state of permanent cell cycle arrest. It is commonly believed to underlie organismal aging and age-associated diseases. However, the mechanism by which cellular senescence contributes to aging and age-associated pathologies remains unclear. Recent studies showed that senescent cells exert detrimental effects on the tissue microenvironment, generating pathological facilitators or aggravators. The most significant environmental effector resulting from senescent cells is the senescence-associated secretory phenotype (SASP), which is constituted by a strikingly increased expression and secretion of diverse pro-inflammatory cytokines. Careful investigation into the components of SASPs and their mechanism of action, may improve our understanding of the pathological backgrounds of age-associated diseases. In this review, we focus on the differential expression of SASP-related genes, in addition to SASP components, during the progress of senescence. We also provide a perspective on the possible action mechanisms of SASP components, and potential contributions of SASP-expressing senescent cells, to age-associated pathologies.
Indexed as
Identifiers
What OpenQuestion holds
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.