ArticleCell death discovery2018
Kindlin-2 regulates hepatic stellate cells activation and liver fibrogenesis.
Article in Cell death discovery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
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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.
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.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Article
- Modeling hepatic fibrosis in TP53 knockout iPSC-derived human liver organoids.Molecular oncology · 2026Article
- Unraveling risk factors and transcriptomic signatures in liver cancer progression and mortality through machine learning and bioinformatics.Briefings in functional genomics · 2026Article
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- Exploring the Therapeutic Potential of TGF-β Inhibitors for Liver Fibrosis: Targeting Multiple Signaling Pathways.Journal of clinical and translational hepatology · 2025Review
- Fibulin-1 deficiency alleviates liver fibrosis by inhibiting hepatic stellate cell activation via the p38 MAPK pathway.Cellular and molecular life sciences : CMLS · 2025Article
- Liver diseases: epidemiology, causes, trends and predictions.Signal transduction and targeted therapy · 2025Review
- Liver-targeted degradation of BRD4 reverses hepatic fibrosis and enhances metabolism in murine models.Theranostics · 2025Article
- Targeting Kindlin-2 in adipocytes increases bone mass through inhibiting FAS/PPARActa pharmaceutica Sinica. B · 2023Article
- The Dual Therapeutic Potential of Ottelione A on Carbon Tetrachloride-induced Hepatic Toxicity in Mice.Applied biochemistry and biotechnology · 2023Article
- Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2023Review
- Targeting TGF-β signal transduction for fibrosis and cancer therapy.Molecular cancer · 2022Review
- Kindlin-2 haploinsufficiency protects against fatty liver by targeting Foxo1 in mice.Nature communications · 2022Article
- YBX1 knockdown induces renal cell carcinoma cell apoptosis via Kindlin-2.Cell cycle (Georgetown, Tex.) · 2021Article
- Integrin β1 Promotes Pancreatic Tumor Growth by Upregulating Kindlin-2 and TGF-β Receptor-2.International journal of molecular sciences · 2021Article
- JNK and p38 Inhibitors Prevent Transforming Growth Factor-β1-Induced Myofibroblast Transdifferentiation in Human Graves' Orbital Fibroblasts.International journal of molecular sciences · 2021Article
- Inhibition of 5-Lipoxygenase in Hepatic Stellate Cells Alleviates Liver Fibrosis.Frontiers in pharmacology · 2021Article
- Article
- Physiopathology of Lifestyle Interventions in Non-Alcoholic Fatty Liver Disease (NAFLD).Nutrients · 2020Review
- Role of Kindlin-2 in cancer progression and metastasis.Annals of translational medicine · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis, the common response associated with chronic liver diseases, ultimately leads to cirrhosis, a major public health problem worldwide. Activation of hepatic stellate cells (HSCs) by transforming growth factor (TGF)-β1 is a key step in liver fibrosis. Here we report that Kindlin-2 expression is elevated in the livers of mice with experimental liver fibrosis and also in the livers of patients with liver fibrosis. TGF-β1 increases Kindlin-2 expression in cultured HSCs in a p38 and ERK mitogen-activated protein kinase (MAPK)-dependent manner, partly. More importantly, Kindlin-2 deficiency significantly attenuated mouse liver fibrosis and HSC activation. Mechanistically, Kindlin-2 promotes TGF-β signaling through upregulation of Smad2 and Smad3 phosphorylation. Our work demonstrates an important role for Kindlin-2 in liver fibrosis, and inhibiting Kindlin-2 in the livers may represent a novel strategy to treat liver fibrosis.
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.