ArticleMolecular medicine (Cambridge, Mass.)2021
IL-17 deficiency aggravates the streptozotocin-induced diabetic nephropathy through the reduction of autophagosome formation in mice.
Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Circulating IL-17 reduces the risk of cisplatin-induced hearing loss in children: a bidirectional two-sample Mendelian randomization study.Scientific reports · 2023Pooled it
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- Molecular mechanisms and novel therapeutic targets of diabetic kidney disease.Chinese medical journal · 2026Review
- Interleukin-17 A and diabetic kidney disease: emerging evidence on its pathogenic role and targeted modulation.Acta diabetologica · 2026Review
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- Tubular injury in diabetic kidney disease: a focus on regulated cell death.Frontiers in endocrinology · 2026Review
- Integrative Transcriptomic and Metabolomic Analysis Reveals ThatInternational journal of molecular sciences · 2025Article
- Potential of Alkaloids fromCurrent issues in molecular biology · 2025Article
- Therapeutic role of Crateva religiosa in diabetic nephropathy: Insights into key signaling pathways.PloS one · 2025Article
- Macrophages in Focus: Key Drivers and Therapeutic Opportunities in Diabetic Kidney Disease.International journal of biological sciences · 2025Review
- Programmed Cell Death in Diabetic Kidney Disease: Mechanisms and Therapeutic Targeting.Journal of inflammation research · 2025Review
- Suppression of renal crystal formation, inflammation, and fibrosis by blocking oncostatin M receptor β signaling.Scientific reports · 2024Article
- Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions.MedComm · 2024Review
- The critical role of dysregulated autophagy in the progression of diabetic kidney disease.Frontiers in pharmacology · 2022Review
- Identification of Oxidative Stress-Related Biomarkers in Diabetic Kidney Disease.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Screening and Identification of Hub Genes in the Development of Early Diabetic Kidney Disease Based on Weighted Gene Co-Expression Network Analysis.Frontiers in endocrinology · 2022Article
- Autophagy in renal fibrosis: Protection or promotion?Frontiers in pharmacology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic nephropathy (DN) is one of the most important medical complications of diabetes mellitus. Autophagy is an important mediator of pathological response and plays a critical role in inflammation during the progression of diabetic nephropathy. Interleukin (IL)-17A favorably modulates inflammatory disorders including DN. In this study, we examined whether IL-17A deficiency affected the autophagy process in the kidneys of mice with streptozotocin (STZ)-induced DN.
methodsThe autophagic response of IL-17A to STZ-induced nephrotoxicity was evaluated by analyzing STZ-induced functional and histological renal injury in IL-17A knockout (KO) mice.
resultsIL-17A KO STZ-treated mice developed more severe nephropathy than STZ-treated wild-type (WT) mice, with increased glomerular damage and renal interstitial fibrosis at 12 weeks. IL-17A deficiency also increased the up-regulation of proinflammatory cytokines and fibrotic gene expression after STZ treatment. Meanwhile, autophagy-associated proteins were induced in STZ-treated WT mice. However, IL-17A KO STZ-treated mice displayed a significant decrease in protein expression. Especially, the levels of LC3 and ATG7, which play crucial roles in autophagosome formation, were notably decreased in the IL-17A KO STZ-treated mice compared with their WT counterparts.
conclusionsIL-17 deficiency aggravates of STZ-induced DN via attenuation of autophagic response. Our study demonstrated that IL-17A mediates STZ-induced renal damage and represents a potential therapeutic target in DN.
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