ArticleInternational journal of clinical and experimental medicine2015
Follistatin-like 3 suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- FGF9 promotes cell proliferation and tumorigenesis in TM3 mouse Leydig progenitor cells.American journal of cancer research · 2022Article
- Follistatin-Like Proteins: Structure, Functions and Biomedical Importance.Biomedicines · 2021Review
- Effect of sericin on the p38MAPK signaling pathway and NLRP3 inflammasome in the kidney of type 2 diabetic rats.Experimental and therapeutic medicine · 2020Article
- Inhibition of NADPH Oxidase 5 (NOX5) Suppresses High Glucose-Induced Oxidative Stress, Inflammation and Extracellular Matrix Accumulation in Human Glomerular Mesangial Cells.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Caveolin-1 regulation of Sp1 controls production of the antifibrotic protein follistatin in kidney mesangial cells.Cell communication and signaling : CCS · 2019Article
- FGF9/FGFR2 increase cell proliferation by activating ERK1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells.Cancer science · 2018Article
- Thymoquinone Alleviates the Experimental Diabetic Peripheral Neuropathy by Modulation of Inflammation.Scientific reports · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mesangial cells (MCs) proliferation and extracellular matrix (ECM) accumulation are early features of diabetic nephropathy. Follistatin-like 3 (FSTL3), a member of follistatin family, has been shown to regulate insulin and glucagon sensitivities in diet-induced obesity and insulin resistance. However, the role of FSTL3 in diabetic nephropathy is still unclear. Therefore, in this study, we investigated the effects of FSTL3 on cell proliferation and ECM accumulation expression in rat MCs cultured under high glucose, and elucidated the underlying mechanism. We found that the expression of FSTL3 was decreased significantly in MCs cultured high glucose condition. Overexpression of FSTL3 inhibited high glucose-induced MC proliferation and blocked the G1/S phase transition under high glucose condition. And, FSTL3 overexpression also reduced the expression of α-smooth muscle actin (α-SMA) and fibronectin (FN) induced by high glucose. Furthermore, overexpression of FSTL3 suppressed high-glucose-induced p38 phosphorylation in MCs. Taken together, our present study demonstrated that FSTL3 suppressed high glucose-induced MC proliferation and ECM accumulation via inhibiting the p38MAPK signaling pathway, and that FSTL3 may be a potential therapeutic target for the treatment of diabetic nephropathy.
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26629006PMC4658895W2182180639What 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.