ArticleScientific reports2019
MG132 protects against renal dysfunction by regulating Akt-mediated inflammation in diabetic nephropathy.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- NEDD4L knockdown enhances synovial fibroblast migration, invasion, and inflammatory factor secretion via Wnt/β-Catenin signaling activation.Clinical rheumatology · 2026Article
- MG132 induces cell type‑specific anticancer effects in uterine leiomyosarcoma cell lines.Molecular medicine reports · 2025Article
- Renal Implications of Dysregulated Protein Homeostasis: Insights into Ubiquitin-Proteasome and Autophagy Systems.Biomolecules · 2025Review
- Baicalin: a potential therapeutic agent for acute kidney injury and renal fibrosis.Frontiers in pharmacology · 2025Review
- The roles of the ubiquitin-proteasome system in renal disease.International journal of medical sciences · 2025Review
- Modeling SILAC Data to Assess Protein Turnover in a Cellular Model of Diabetic Nephropathy.International journal of molecular sciences · 2023Article
- The Preeclamptic Environment Promotes the Activation of Transcription Factor Kappa B by P53/RSK1 Complex in a HTR8/SVneo Trophoblastic Cell Line.International journal of molecular sciences · 2021Article
- Role of Dendritic Cell in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- LncRNA lnc-ISG20 promotes renal fibrosis in diabetic nephropathy by inducing AKT phosphorylation through miR-486-5p/NFAT5.Journal of cellular and molecular medicine · 2021Article
- Moxibustion Inhibits the Expression of Colonic NLRP3 through miR7/RNF183/NF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Magnoflorine Ameliorates Inflammation and Fibrosis in Rats With Diabetic Nephropathy by Mediating the Stability of Lysine-Specific Demethylase 3A.Frontiers in physiology · 2020Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN), the leading cause of end-stage renal disease (ESRD). To date, mounting evidence has shown that inflammation may contribute to the pathogenesis of DN. Recent reports have shown that proteasome inhibitors display cytoprotection by reducing the phosphorylation of Akt, a serine/threonine kinase, plays a critical role in cellular survival and metabolism and can crosstalk with inflammation. Therefore, we hypothesized that MG132, specific proteasome inhibitor, could provide renoprotection by suppressing Akt-mediated inflammation in DN. In vivo, male Sprague-Dawley rats were divided into normal control group (NC), diabetic nephropathy group (DN), DN model plus MG132 treatment group (MG132), and DN model plus deguelin treatment group (Deguelin)(deguelin, a specific inhibitor of Akt). In vitro, a human glomerular mesangial cell lines (HMCs) was exposed to 5.5 mmol/L glucose (CON), 30 mmol/L glucose (HG), 30 mmol/L glucose with 0.5 umol/L MG132 (MG132) and 30 mmol/L glucose with 5 umol/L deguelin (Deguelin). Compared with NC, DN showed a significant increase in the urinary protein excretion rate and inflammatory cytokines, as well as p-Akt. Compared with CON, HMCs co-cultured with HG was notably proliferated, which is in accord with α-smooth muscle actin (α-SMA) expression. These alterations were inhibited by administration of MG132 or deguelin. In conclusion, MG132 significantly inhibits the development of DN by regulating Akt phosphorylation-mediated inflammatory activation.
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