ArticleAging cell2022
Dynamic regulation of myofibroblast phenotype in cellular senescence.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Mesothelial cell senescence induced by high glucose in peritoneal dialysis drives fibroblast activation and peritoneal fibrosis through KLF6-mediated activation of TGF-β pathway.Molecular and cellular biochemistry · 2026Article
- Resolvin D1 attenuates senescence-associated secretory phenotype independently of TGF-β-driven cardiac fibroblasts differentiation to myofibroblast.Journal of inflammation (London, England) · 2026Article
- Radiomitigators: Breakthroughs in Post-Radiation Recovery.Antioxidants (Basel, Switzerland) · 2026Review
- Fibroblast growth factor-inducible 14 accelerates pulmonary fibrosis by inducing fibroblast senescence in mice.Cellular and molecular life sciences : CMLS · 2026Article
- STL1267 inhibits myofibroblast differentiation in a TGFβ1-driven human lung fibroblast model.American journal of physiology. Cell physiology · 2026Article
- Mapping the Progression of Therapy-Induced Senescence to Therapy Tolerance: An Evolutionarily Conserved Mechanism for Optimizing Cancer Treatment with Senotherapeutics.ACS pharmacology & translational science · 2025Article
- Emerging Perspectives in Anti-aging Treatments Using Anti-Fibrotic Strategies.Aging and disease · 2025Review
- The Role of Mitochondria-Associated Endoplasmic Reticulum Membranes in Fibrotic Diseases.Aging and disease · 2025Review
- Involvement of TGF-β, mTOR, and inflammatory mediators in aging alterations during myxomatous mitral valve disease in a canine model.GeroScience · 2025Review
- Cells of all trades - on the importance of spatial positioning of senescent cells in development, healing and aging.FEBS letters · 2025Review
- A Distinguished Roadmap of Fibroblast Senescence in Predicting Immunotherapy Response and Prognosis Across Human Cancers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting senescence to prevent diabetic kidney disease: Exploring molecular mechanisms and potential therapeutic targets for disease management.Diabetic medicine : a journal of the British Diabetic Association · 2025Review
- Idiopathic epiretinal membrane area changes in eyes with good vision and the association with visual function.PloS one · 2025Article
- Non-immune factors cause prolonged myofibroblast phenotype in implanted synthetic heart valve scaffolds.Applied materials today · 2024Article
- Senescence-Associated Alterations in Matrisome of Mesenchymal Stem Cells.International journal of molecular sciences · 2024Article
- Retrospective identification of cell-intrinsic factors that mark pluripotency potential in rare somatic cells.Cell systems · 2024Article
- AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration.Biogerontology · 2024Review
- Systematic transcriptomic analysis and temporal modelling of human fibroblast senescence.Frontiers in aging · 2024Article
- Article
- Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype.Nature metabolism · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is an antiproliferative response with a critical role in the control of cellular balance in diverse physiological and pathological settings. Here, we set to study the impact of senescence on the regulation of cell plasticity, focusing on the regulation of the myofibroblastic phenotype in primary fibroblasts. Myofibroblasts are contractile, highly fibrogenic cells with key roles in wound healing and fibrosis. Using cellular models of fibroblast senescence, we find a consistent loss of myofibroblastic markers and functional features upon senescence implementation. This phenotype can be transmitted in a paracrine manner, most likely through soluble secreted factors. A dynamic transcriptomic analysis during paracrine senescence confirmed the non-cell-autonomous transmission of this phenotype. Moreover, gene expression data combined with pharmacological and genetic manipulations of the major SASP signaling pathways suggest that the changes in myofibroblast phenotype are mainly mediated by the Notch/TGF-β axis, involving a dynamic switch in the TGF-β pathway. Our results reveal a novel link between senescence and myofibroblastic differentiation with potential implications in the physiological and pathological functions of myofibroblasts.
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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.