ArticleLife sciences2021
ERK and p38 MAPK inhibition controls NF-E2 degradation and profibrotic signaling in renal proximal tubule cells.
Article in Life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- The inflammatory-autophagy-NETs axis in renal fibrosis: mechanistic crosstalk and pathological feed-forward amplification loops.Molecular and cellular biochemistry · 2026Review
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- The subcellular localization-dependent dual role of NR4A1 in renal fibrosis: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Field direction of static magnetic fields influences kidney fibrosis progression through MAPK signaling and cell cycle alteration.Scientific reports · 2025Article
- Article
- Analysis of the potential biological mechanisms of geniposide on renal fibrosis by network pharmacology and experimental verification.BMC pharmacology & toxicology · 2025Article
- Baricitinib in chronic kidney disease: an exploratory analysis integrating network toxicology, molecular docking and pharmacovigilance.Frontiers in medicine · 2025Article
- STAP2 promotes the progression of renal fibrosis via HSP27.Journal of translational medicine · 2024Article
- Integrating network pharmacology and experimental validation to decipher the mechanism of the Chinese herbal prescription modified Shen-Yan-Fang-Shuai formula in treating diabetic nephropathy.Pharmaceutical biology · 2023Article
- Dual specificity phosphatase 22 suppresses mesangial cell hyperproliferation, fibrosis, inflammation and the MAPK signaling pathway in diabetic nephropathy.Experimental and therapeutic medicine · 2022Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
aimsTransforming growth factor-β (TGF-β) mediates fibrotic manifestations of diabetic nephropathy. We demonstrated proteasomal degradation of anti-fibrotic protein, nuclear factor-erythroid derived 2 (NF-E2), in TGF-β treated human renal proximal tubule (HK-11) cells and in diabetic mouse kidneys. The current study examined the role of mitogen-activated protein kinase (MAPK) pathways in mediating NF-E2 proteasomal degradation and stimulating profibrotic signaling in HK-11 cells. MAIN
methodsHK-11 cells were pretreated with vehicle or appropriate proteasome and MAPK inhibitors, MG132 (0.5 μM), SB203580 (1 μM), PD98059 (25 μM) and SP600125 (10 μM), respectively, followed by treatment with/without TGF-β (10 ng/ml, 24 h). Cell lysates and kidney homogenates from FVB and OVE26 mice treated with/without MG132 were immunoblotted with appropriate antibodies. pUse vector and pUse-NF-E2 cDNA were transfected in HK-11 cells and effects of TGF-β on JNK MAPK phosphorylation (pJNK) was examined. KEY
findingsWe demonstrated activation of p38, ERK, and JNK MAPK pathways in TGF-β treated HK-11 cells. Dual p38 and ERK MAPK blockade prevented TGF-β-induced pSer SIGNIFICANCE: ERK and p38 MAPK promotes NF-E2 proteasomal degradation while proteasome activation promotes pJNK and profibrotic signaling in renal proximal tubule cells.
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