ArticleJournal of cellular and molecular medicine2012
Senescence determines the fate of activated rat pancreatic stellate cells.
Article in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 64 citations in OpenAlex.
- Harnessing the NKG2D immune surveillance pathway using engineered T-cells for the treatment of human disease.Human vaccines & immunotherapeutics · 2026Review
- Age-dependent elevation of Nr4a1 attenuates PI3K/AKT/GSK3β pathway and mediates tau hyperphosphorylation and cognitive impairments.Journal of advanced research · 2026Article
- Modelling the spatiotemporal dynamics of senescent cells in wound healing, chronic wounds, and fibrosis.PLoS computational biology · 2025Article
- Alterations in exocrine pancreatic function after acute pancreatitis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2024Review
- Senescence program and its reprogramming in pancreatic premalignancy.Cell death & disease · 2023Review
- Biomarkers of aging.Science China. Life sciences · 2023Review
- Changes in Pancreatic Senescence Mediate Pancreatic Diseases.International journal of molecular sciences · 2023Review
- Mettl14-driven senescence-associated secretory phenotype facilitates somatic cell reprogramming.Stem cell reports · 2022Article
- The Senescence Markers p16INK4A, p14ARF/p19ARF, and p21 in Organ Development and Homeostasis.Cells · 2022Review
- Pancreatic Cancer and Cellular Senescence: Tumor Microenvironment under the Spotlight.International journal of molecular sciences · 2021Review
- Myofibroblast fate plasticity in tissue repair and fibrosis: Deactivation, apoptosis, senescence and reprogramming.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2021Article
- Article
- Cellular senescence in ageing: from mechanisms to therapeutic opportunities.Nature reviews. Molecular cell biology · 2021Review
- Immune Aging and How It Works for Inflammation and Fibrosis.Frontiers in physiology · 2021Review
- Cellular senescence: friend or foe to respiratory viral infections?The European respiratory journal · 2020Article
- Retinoids in Stellate Cells: Development, Repair, and Regeneration.Journal of developmental biology · 2019Review
- Systemic inflammation contributes to impairment of quality of life in chronic pancreatitis.Scientific reports · 2019Observational
- Review
- Targeting Senescent Cells in Fibrosis: Pathology, Paradox, and Practical Considerations.Current rheumatology reports · 2018Review
- A Rising Star in Pancreatic Diseases: Pancreatic Stellate Cells.Frontiers in physiology · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In chronic pancreatitis (CP), persistent activation of pancreatic stellate cells (PSC) converts wound healing into a pathological process resulting in organ fibrosis. Here, we have analysed senescence as a novel mechanism involved in the termination of PSC activation and tissue repair. PSC senescence was first studied in vitro by establishing long-term cultures and by applying chemical triggers, using senescence-associated β-Galactosidase (SA β-Gal) as a surrogate marker. Subsequently, susceptibility of PSC to immune cell-mediated cytolysis was investigated employing cocultures. Using the model of dibutyltin dichloride-induced CP in rats, appearance of senescent cells was monitored by immunohistochemistry and immunofluorescence, and correlated with the progression of tissue damage and repair, immune cell infiltration and fibrosis. The results indicated that long-term culture and exposure of PSC to stressors (doxorubicin, H(2) O(2) and staurosporine) induced senescence. Senescent PSC highly expressed CDKN1A/p21, mdm2 and interleukin (IL)-6, but displayed low levels of α-smooth muscle actin. Senescence increased the susceptibility of PSC to cytolysis. In CP, the number of senescent cells correlated with the severity of inflammation and the extension of fibrosis. Areas staining positive for SA β-Gal overlapped with regions of fibrosis and dense infiltrates of immune cells. Furthermore, a close physical proximity of immune cells and activated PSC was observed. We conclude that inflammation, PSC activation and cellular senescence are timely coupled processes which take place in the same microenvironment of the inflamed pancreas. Lymphocytes may play a dual-specific role in pancreatic fibrogenesis, triggering both the initiation of wound healing by activating PSC, and its completion by killing senescent stellate cells.
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.