ArticleMolecular biology reports2010
Aldose reductase is a potent regulator of TGF-β1 induced expression of fibronectin in human mesangial cells.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Protective Effects of Ethanolic Extract from Rhizome ofInternational journal of molecular sciences · 2021Article
- Role of aldose reductase in diabetes-induced retinal microglia activation.Chemico-biological interactions · 2019Article
- Amelioration of Bleomycin-induced Pulmonary Fibrosis of Rats by an Aldose Reductase Inhibitor, Epalrestat.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Article
- Lignans from the bark of Eucommia ulmoides inhibited Ang II-stimulated extracellular matrix biosynthesis in mesangial cells.Chinese medicine · 2014Article
- A potential therapeutic role for aldose reductase inhibitors in the treatment of endotoxin-related inflammatory diseases.Expert opinion on investigational drugs · 2012Review
- Aldo-Keto Reductases: Multifunctional Proteins as Therapeutic Targets in Diabetes and Inflammatory Disease.Advances in experimental medicine and biologyReview
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5 authors at 1 institution in 1 country.
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Abstract
Glomerulosclerosis is considered to be the final pathway leading to the progressive loss of renal function in several kidney diseases, transforming growth factor β1 (TGF-β1) plays a critical role in glomerulosclerosis. However, the mechanisms of TGF-β1 stimulating glomerulosclerosis remain poorly understood. Here we report that TGF-β1-induced expression of fibronectin (FN) depends on the activity of aldose reductase (AR) in human mesangial cells (HMCs).The results show that TGF-β1 increased the expression of FN, which attenuated by pharmacological inhibition of AR or knockdown of the enzyme by small interfering RNA (siRNA). MAPKs (ERK, JNK and p38) signalling pathways were activated in HMCs after stimulated by TGF-β1, inhibition of AR blunted the activation ERK, p38 and JNK signalling pathways. These changes were associated with decreased TGF-β1-induced expression of FN. These results indicate that AR is a potent regulator of TGF-β1 induced expression of FN in human mesangial cells: it suggests that inhibition of this enzyme may be useful to prevented extracellular matrix (ECM) deposition in glomerulosclerosis.
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