ArticleFrontiers in cell and developmental biology2021
Integrin β3 Induction Promotes Tubular Cell Senescence and Kidney Fibrosis.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 22 citations in OpenAlex.
- Uncovering potential biomarkers for chronic kidney disease of unknown etiology through a network-based bioinformatic approach.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Polysaccharide Peptide fromBiomolecules · 2026Article
- Multi-Omics Alterations in Rat Kidneys upon Chronic Glyphosate Exposure.Biomolecules · 2025Article
- Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease.Cell death & disease · 2025Article
- Cellular and Molecular Resolution of Focal Segmental Glomerulosclerosis Recurrence in Human Allografts.bioRxiv : the preprint server for biology · 2025Article
- Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.Frontiers of medicine · 2025Review
- Supplementation of 18β-glycyrrhetinic acid attenuates D-galactose-induced oxidative stress and inflammatory responses in kidneys of weaned piglet.Journal of animal science · 2025Article
- Factor XII signaling via uPAR-integrin β1 axis promotes tubular senescence in diabetic kidney disease.Nature communications · 2024Article
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- C-X-C chemokine receptor type 4 promotes tubular cell senescence and renal fibrosis through β-catenin-inhibited fatty acid oxidation.Journal of cellular and molecular medicine · 2024Article
- Obstructive nephropathy and molecular pathophysiology of renal interstitial fibrosis.Physiological reviews · 2023Review
- Integrin beta 3-overexpressing mesenchymal stromal cells display enhanced homing and can reduce atherosclerotic plaque.World journal of stem cells · 2023Article
- Article
- The Therapeutic Mechanism of Schisandrol A and Its Metabolites on Pulmonary Fibrosis Based on Plasma Metabonomics and Network Analysis.Drug design, development and therapy · 2023Article
- Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease.International journal of molecular sciences · 2022Review
- ZNF281 Promotes Colon Fibroblast Activation in TGFβ1-Induced Gut Fibrosis.International journal of molecular sciences · 2022Article
- Natural products: potential drugs for the treatment of renal fibrosis.Chinese medicine · 2022Review
- Role of MMP-2 and CD147 in kidney fibrosis.Open life sciences · 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
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tubular cell senescence is a common biologic process and contributes to the progression of chronic kidney disease (CKD); however, the molecular mechanisms regulating tubular cell senescence are poorly understood. Here, we report that integrin β3 (ITGB3) expression was increased in tubular cells and positively correlated with fibrosis degree in CKD patients. ITGB3 overexpression could induce p53 pathway activation and the secretion of TGF-β, which, in turn, resulted in senescent and profibrotic phenotype change in cultured tubular cells. Moreover, according to the CMAP database, we identified isoliquiritigenin (ISL) as an agent to inhibit ITGB3. ISL treatment could suppress Itgb3 expression, attenuate cellular senescence, and prevent renal fibrosis in mice. These results reveal a crucial role for integrin signaling in cellular senescence, potentially identifying a new therapeutic direction for kidney fibrosis.
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.