ReviewCellular and molecular life sciences : CMLS2018
Cellular senescence: a view throughout organismal life.
Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 68 citations in OpenAlex.
- Oxidative stress promotes the progression of age-related macular degeneration by up-regulating Spp1 to activate the JAK/STAT signaling pathway.Scientific reports · 2026Article
- The puzzling duality of mesenchymal stem cells and adipocytes in bone marrow and ageing.npj aging · 2026Review
- PDZK1 Protects Against RPE Senescence by Targeting the 14-3-3ε-mTOR Axis to Attenuate Early Diabetic Retinopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- Cells of all trades - on the importance of spatial positioning of senescent cells in development, healing and aging.FEBS letters · 2025Review
- A Functional Skincare Formulation Mixed With Retinyl Propionate, Hydroxypinacolone Retinoate, and Vitamin C on Antiaging and Whitening Han Women in Shanghai, China.Journal of cosmetic dermatology · 2025Article
- Chemotherapy-induced cellular senescence promotes stemness of aggressive B-cell non-Hodgkin's lymphoma via CCR7/ARHGAP18/IKBα signaling activation.Journal for immunotherapy of cancer · 2025Article
- Factors negatively affecting quality of life in geriatric patients: review.GMS hygiene and infection control · 2025Review
- Review of evidence linking exposure to environmental stressors and associated alterations in the dynamics of immunosenescence (ISC) with the global increase in multiple sclerosis (MS).Immunity & ageing : I & A · 2024Review
- HDAC4 influences the DNA damage response and counteracts senescence by assembling with HDAC1/HDAC2 to control H2BK120 acetylation and homology-directed repair.Nucleic acids research · 2024Article
- Stress Hormones: Unveiling the Role in Accelerated Cellular Senescence.Aging and disease · 2024Review
- Revolutionizing Diabetic Foot Ulcer Care: The Senotherapeutic Approach.Aging and disease · 2024Review
- A common molecular and cellular pathway in developing Alzheimer and cancer.Biochemistry and biophysics reports · 2024Review
- Age-Related Macular Degeneration: A Disease of Cellular Senescence and Dysregulated Immune Homeostasis.Clinical interventions in aging · 2024Review
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- Immunotherapeutic approach to reduce senescent cells and alleviate senescence-associated secretory phenotype in mice.Aging cell · 2023Article
- DNA Damage Response-Associated Cell Cycle Re-Entry and Neuronal Senescence in Brain Aging and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Potential Role of Polyphenolic Flavonoids as Senotherapeutic Agents in Degenerative Diseases and Geroprotection.Pharmaceutical medicine · 2022Review
- Oxidative Stress-Induced Cellular Senescence in Aging Retina and Age-Related Macular Degeneration.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is the final fate of most cells in response to specific stimuli, but is not the end. Indeed, it is the beginning of a singular life, with multiple side roads leading to diverse effects on the organism. Many studies have been done in the last few years to elucidate the intriguing role of senescent cells in the organism, demonstrating them as the cause of several age-related diseases. However, these cells are also positively implicated in other important pathways, such as embryogenesis and wound healing. It appears that the multiple effects are time-dependent: long-term senescence is mostly implicated in chronic inflammation and disease, whereas in the short term, senescent cells seem to be beneficial, being rapidly targeted by the innate immune system. The influence of senescent cells on their neighbors by paracrine factors, differential activity depending on developmental stage, and duration of the effects make the cellular senescent program a unique spatial-temporal mechanism. During pathological conditions such as progeroid syndromes, this mechanism is deregulated, leading to accelerated onset of some aging-related diseases and a shorter lifespan, among other physiological defects. Here, we review the three primary cell senescence programs described so far (replicative, stress-induced, and developmentally programmed senescence), their onset during development, and their potential roles in diseases with premature aging. Finally, we discuss the role of immune cells in keeping senescence burden below the threshold of disease.
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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.