ArticleMolecular and cellular biochemistry2012
STAT1 mediates cellular senescence induced by angiotensin II and H₂O₂ in human glomerular mesangial cells.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 33 citations in OpenAlex.
- Dual Functions of B7-H3-MAPK Signaling Orchestrate Tumor Immunosuppression via Regulating the Plasticity of Myeloid-derived Suppressor Cells and Fibroblasts.Cancer discovery · 2026Article
- Dietary Lauric Acid Suppresses Inflammation, Cholestasis, Hepatocyte Injury, and Senescence in 3,5-Diethoxycarbonyl-1,4-Dihydrocollidine-induced Inflammatory Cholangiopathy.Cellular and molecular gastroenterology and hepatology · 2026Article
- Aging associated immunosenescence in rheumatoid arthritis identified by machine learning and single cell profiling.Scientific reports · 2025Article
- SIRT7 regulates NUCKS1 chromatin binding to elicit metabolic and inflammatory gene expression in senescence and liver aging.Molecular cell · 2025Article
- Chronic kidney disease and aging: dissecting the p53/p21 pathway as a therapeutic target.Biogerontology · 2024Review
- Phylloquinone improves endothelial function, inhibits cellular senescence, and vascular inflammation.GeroScience · 2024Article
- Article
- JAK/STAT signaling in diabetic kidney disease.Frontiers in cell and developmental biology · 2023Review
- Progeria and Aging-Omics Based Comparative Analysis.Biomedicines · 2022Article
- BMP9 reduces age-related bone loss in mice by inhibiting osteoblast senescence through Smad1-Stat1-P21 axis.Cell death discovery · 2022Article
- Gut-kidney axis in IgA nephropathy: Role on mesangial cell metabolism and inflammation.Frontiers in cell and developmental biology · 2022Review
- Senescent T cells within suppressive tumor microenvironments: emerging target for tumor immunotherapy.The Journal of clinical investigation · 2020Review
- The Signaling of Cellular Senescence in Diabetic Nephropathy.Oxidative medicine and cellular longevity · 2019Review
- Mechanisms of carbon nanotube-induced pulmonary fibrosis: a physicochemical characteristic perspective.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018Review
- Regulatory T cells trigger effector T cell DNA damage and senescence caused by metabolic competition.Nature communications · 2018Article
- Targeted inhibition of STATs and IRFs as a potential treatment strategy in cardiovascular disease.Oncotarget · 2016Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human glomerular mesangial cells (HMCs) have a finite lifespan and eventually enter irreversible growth arrest known as cellular senescence which is thought to contribute to kidney aging and age-related kidney disorders, such as chronic kidney disease. The signal transducer and activator of transcription 1 (STAT1) is a latent transcription factor involved in a variety of signal transduction pathways, including cell proliferation, apoptosis, and differentiation, but whether it could regulate HMCs senescence still remains to be explored. In our study, induction of Angiotensin II (Ang II) and H(2)O(2) accelerated premature senescence of HMCs as confirmed by increased senescence-associated -β-galactosidase (SA-β-gal) positive staining cells and G0/G1 cell cycle arrest. The STAT1 and STAT3 activity and the expression of p53 and p21(Cip1) were increased after Angiotensin II and H(2)O(2) treatment. Knockdown STAT1 using RNA interference significantly attenuated the progression of HMCs senescence, decreased the elevated p53 and p21(Cip1), more interestingly, STAT3 and its activity was further enhanced while STAT1 was silenced. Our results indicate that STAT1 might mediate Ang II and H(2)O(2)-induced HMCs senescence through p53/p21(Cip1) pathway and the relative abundance of STAT1 and STAT3.
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.