ArticleActa pharmacologica Sinica2018
SND p102 promotes extracellular matrix accumulation and cell proliferation in rat glomerular mesangial cells via the AT1R/ERK/Smad3 pathway.
Article in Acta pharmacologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 23 citations in OpenAlex.
- Dysregulation of miR-25-3p in Diabetic Nephropathy and Its Role in Inflammatory Response.Biochemical genetics · 2025Article
- Bridging Cancer and COVID-19: The Complex Interplay of ACE2 and TMPRSS2.Cancer medicine · 2025Review
- Cytosolic Hmgb1 accumulation in mesangial cells aggravates diabetic kidney disease progression via NFκB signaling pathway.Cellular and molecular life sciences : CMLS · 2024Article
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- LncRNA 1500026H17Rik knockdown ameliorates high glucose-induced mouse podocyte injuries through the miR-205-5p/EGR1 pathway.International urology and nephrology · 2023Article
- Renal function protection and the mechanism of ginsenosides: Current progress and future perspectives.Frontiers in pharmacology · 2023Review
- A Cyclopentanone Compound Attenuates the Over-Accumulation of Extracellular Matrix and Fibrosis in Diabetic Nephropathy via Downregulating the TGF-β/p38MAPK Axis.Biomedicines · 2022Article
- RAAS, ACE2 and COVID-19; a mechanistic review.Saudi journal of biological sciences · 2021Review
- LncRNA HCP5 knockdown inhibits high glucose-induced excessive proliferation, fibrosis and inflammation of human glomerular mesangial cells by regulating the miR-93-5p/HMGA2 axis.BMC endocrine disorders · 2021Article
- Up-regulation of MMP-2 by histone H3K9 β-hydroxybutyrylation to antagonize glomerulosclerosis in diabetic rat.Acta diabetologica · 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
- BKInternational journal of endocrinology · 2020Article
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10 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
SND p102 was first described as a transcriptional co-activator, and subsequently determined to be a co-regulator of Pim-1, STAT6 and STAT5. We previously reported that SND p102 expression was increased in high glucose-treated mesangial cells (MCs) and plays a role in the extracellular matrix (ECM) accumulation of MCs by regulating the activation of RAS. In this study, we further examined the roles of SND p102 in diabetic nephropathy (DN)-induced glomerulosclerosis. Rats were injected with STZ (50 mg/kg, ip) to induce diabetes. MCs or isolated glomeruli were cultured in normal glucose (NG, 5.5 mmol/L)- or high glucose (HG, 25 mmol/L)-containing DMEM. We found that SND p102 expression was significantly increased in the diabetic kidneys, as well as in HG-treated isolated glomeruli and MCs. In addition, HG treatment induced significant fibrotic changes in MCs evidenced by enhanced protein expression of TGF-β, fbronectin and collagen IV, and significantly increased the proliferation of MCs. We further revealed that overexpression of SND p102 significantly increased the protein expression of angiotensin II (Ang II) type 1 receptor (AT1R) in MCs by increasing its mRNA levels via directly targeting the AT1R 3'-UTR, which resulted in activation of the ERK/Smad3 signaling and subsequently promoted the up-regulation of fbronectin, collagen IV, and TGF-β in MCs, as well as the cell proliferation. These results demonstrate that SND p102 is a key regulator of AT1R-mediating ECM synthesis and cell proliferation in MCs. Thus, small molecule inhibitors of SND p102 may be a novel therapeutic strategy for DN.
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