ArticleMolecular medicine reports2020
DUSP6 protects murine podocytes from high glucose‑induced inflammation and apoptosis.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Biomimetic fractal topography enhances podocyte maturation in vitro.Nature communications · 2025Article
- Preventive regulation of cellular heat stress injury by mung bean polyphenols revealed by multi-omics analysis.NPJ science of food · 2025Article
- Cordycepin ameliorates diabetic nephropathy injury by activating the SLC7A11/GPX4 pathway.Journal of diabetes investigation · 2025Article
- β-Sitosterol Mitigates Apoptosis, Oxidative Stress and Inflammatory Response by Inactivating TLR4/NF-кB Pathway in Cell Models of Diabetic Nephropathy.Cell biochemistry and biophysics · 2025Article
- The role of ERK1/2 signaling in diabetes: pathogenic and therapeutic implications.Frontiers in pharmacology · 2025Review
- Sevoflurane augments neuroinflammation by regulating DUSP6 via YTHDF1 in postoperative cognitive dysfunction.Toxicology research · 2024Article
- LncTUG1 ameliorates renal tubular fibrosis in experimental diabetic nephropathy through the miR-145-5p/dual-specificity phosphatase 6 axis.Renal failure · 2023Article
- Poricoic acid A induces mitophagy to ameliorate podocyte injury in diabetic kidney disease via downregulating FUNDC1.Journal of biochemical and molecular toxicology · 2023Article
- Minichromosome maintenance 6 protects against renal fibrogenesis by regulating DUSP6-mediated ERK/GSK-3β/Snail1 signaling.iScience · 2023Article
- ADAM metallopeptidase domain 10 knockdown enables podocytes to resist high glucose stimulation by inhibiting pyroptosis via MAPK pathway.Experimental and therapeutic medicine · 2023Article
- Mycophenolic acid directly protects podocytes by preserving the actin cytoskeleton and increasing cell survival.Scientific reports · 2023Article
- DUSP1 mediates BCG induced apoptosis and inflammatory response in THP-1 cells via MAPKs/NF-κB signaling pathway.Scientific reports · 2023Article
- Identification of common molecular signatures of SARS-CoV-2 infection and its influence on acute kidney injury and chronic kidney disease.Frontiers in immunology · 2023Article
- Targeting protein phosphatases for the treatment of inflammation-related diseases: From signaling to therapy.Signal transduction and targeted therapy · 2022Review
- Overexpression of miR‑375 reverses the effects of dexamethasone on the viability, migration, invasion and apoptosis of human airway epithelial cells by targeting DUSP6.International journal of molecular medicine · 2022Article
- Dual-Specificity Phosphatases and Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the most severe complications that can occur in patients with diabetes, and without effective and timely therapeutic intervention, can gradually progress to renal failure. Previous studies have focused on investigating the pathogenesis of DN; however, the role of dual‑specificity phosphatase 6 (DUSP6) in DN is not completely understood. Therefore, the present study aimed to investigate the role of dual‑specificity phosphatase 6 (DUSP6) in DN. DN model mice were established and the expression levels of DUSP6 in the kidney tissues and high glucose (HG)‑induced murine podocytes (MPC5 cells) were determined using immunohistochemistry, reverse transcription‑quantitative PCR and western blotting. In addition, the levels of reactive oxygen species (ROS) and inflammatory cytokines in MPC5 cells were analyzed using commercial assay kits or ELISA kits, respectively, and flow cytometric analysis was performed to analyze the rate of cell apoptosis. The present study indicated that DUSP6 expression levels were significantly decreased in DN model mice compared with control mice, and in HG‑induced MPC5 cells compared with normal glucose‑induced MPC5 cells. DUSP6 overexpression enhanced MPC5 cell viability and increased protein expression levels of cell markers, such as synaptopodin and nephrin, compared with the negative control group. DUSP6 overexpression also reduced the levels of ROS and inflammatory cytokines, including interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α secreted by MPC5 cells under HG conditions. Moreover, compared with the HG group, cell apoptosis was inhibited by DUSP6 overexpression under HG conditions, which was further indicated by decreased expression levels of cleaved caspase‑3 and Bax. Thus, these findings indicated that DUSP6 mediated the protection against HG‑induced inflammatory response.
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