ArticleBiochimica et biophysica acta. General subjects2017
Soluble epoxide hydrolase in podocytes is a significant contributor to renal function under hyperglycemia.
Article in Biochimica et biophysica acta. General subjects, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Alterations in mitochondria and cellular senescence in aged sEH null female kidneys.GeroScience · 2026Article
- Targeting endoplasmic reticulum stress: an innovative therapeutic strategy for podocyte-related kidney diseases.Journal of translational medicine · 2025Review
- Regulation of soluble epoxide hydrolase in renal-associated diseases: insights from potential mechanisms to clinical researches.Frontiers in endocrinology · 2024Review
- Soluble Epoxide Hydrolase Contributes to Cell Senescence and ER Stress in Aging Mice Colon.International journal of molecular sciences · 2023Article
- Soluble Epoxide Hydrolase and Diabetes Complications.International journal of molecular sciences · 2022Review
- Genetic deficiency or pharmacological inhibition of soluble epoxide hydrolase ameliorates high fat diet-induced pancreatic β-cell dysfunction and loss.Free radical biology & medicine · 2021Article
- Plasma and urinary concentrations of arachidonic acid-derived eicosanoids are associated with diabetic kidney disease.EXCLI journal · 2021Article
- Soluble Epoxide Hydrolase Inhibition byInternational journal of molecular sciences · 2020Article
- Inhibition of soluble epoxide hydrolase attenuates renal tubular mitochondrial dysfunction and ER stress by restoring autophagic flux in diabetic nephropathy.Cell death & disease · 2020Article
- Inactivation of CysBritish journal of pharmacology · 2020Article
- Epoxy Fatty Acids Are Promising Targets for Treatment of Pain, Cardiovascular Disease and Other Indications Characterized by Mitochondrial Dysfunction, Endoplasmic Stress and Inflammation.Advances in experimental medicine and biology · 2020Review
- Serum lncRNA HAND2-AS1 is downregulated in diabetic patients with chronic renal failure and ameliorates cell apoptosis.Diabetology & metabolic syndrome · 2020Article
- Conserved properties of genetic architecture of renal and fat transcriptomes in rat models of insulin resistance.Disease models & mechanisms · 2019Article
- Inhibition of soluble epoxide hydrolase attenuates a high-fat diet-mediated renal injury by activating PAX2 and AMPK.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Oestrogen inhibits PTPRO to prevent the apoptosis of renal podocytes.Experimental and therapeutic medicine · 2019Article
- Article
- Ablation of soluble epoxide hydrolase reprogram white fat to beige-like fat through an increase in mitochondrial integrity, HO-1-adiponectin in vitro and in vivo.Prostaglandins & other lipid mediators · 2018Article
- Inhibition of Soluble Epoxide Hydrolase 2 Ameliorates Diabetic Keratopathy and Impaired Wound Healing in Mouse Corneas.Diabetes · 2018Article
- Inhibition of Soluble Epoxide Hydrolase for Renal Health.Frontiers in pharmacology · 2018Review
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundDiabetic nephropathy (DN) is the leading cause of renal failure, and podocyte dysfunction contributes to the pathogenesis of DN. Soluble epoxide hydrolase (sEH, encoded by Ephx2) is a conserved cytosolic enzyme whose inhibition has beneficial effects on renal function. The aim of this study is to investigate the contribution of sEH in podocytes to hyperglycemia-induced renal injury. MATERIALS AND
methodsMice with podocyte-specific sEH disruption (pod-sEHKO) were generated, and alterations in kidney function were determined under normoglycemia, and high-fat diet (HFD)- and streptozotocin (STZ)-induced hyperglycemia.
resultssEH protein expression increased in murine kidneys under HFD- and STZ-induced hyperglycemia. sEH deficiency in podocytes preserved renal function and glucose control and mitigated hyperglycemia-induced renal injury. Also, podocyte sEH deficiency was associated with attenuated hyperglycemia-induced renal endoplasmic reticulum (ER) stress, inflammation and fibrosis, and enhanced autophagy. Moreover, these effects were recapitulated in immortalized murine podocytes treated with a selective sEH pharmacological inhibitor. Furthermore, pharmacological-induced elevation of ER stress or attenuation of autophagy in immortalized podocytes mitigated the protective effects of sEH inhibition.
conclusionsThese findings establish sEH in podocytes as a significant contributor to renal function under hyperglycemia. GENERAL SIGNIFICANCE: These data suggest that sEH is a potential therapeutic target for podocytopathies.
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