ReviewFrontiers in pharmacology2025
Immunomodulatory roles of quercetin in diabetic nephropathy: targeting inflammation, oxidative stress, and ferroptosis.
Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Integrative multi-omics Mendelian randomization reveals key lipid metabolism genes as therapeutic targets for diabetic nephropathy pathogenesis.Renal failure · 2026Article
- Quercetin as a Multifunctional Flavonol: Molecular Insights and Therapeutic Applications.Molecules (Basel, Switzerland) · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
Diabetic nephropathy (DN) is one of the most common and disabling chronic complications of diabetes, with a complex pathogenesis involving genetic susceptibility, inflammatory responses, oxidative stress, and other pathological processes. Current therapeutic approaches can partially control hyperglycemia and slow the decline of renal function, but remain insufficient to reverse established structural damage to the kidneys. This underscores the urgent need for novel, safe, and multi-targeted intervention strategies. In recent years, natural bioactive compounds have attracted considerable attention for their potential in preventing and treating chronic diseases. Quercetin, a natural flavonoid widely distributed in plants, exhibits multiple biological activities-including anti-inflammatory, antioxidant, anti-fibrotic, and cell death-modulating effects-and has shown significant promise in DN therapy. This review provides a comprehensive overview of the major pathogenic mechanisms of DN and recent advances in understanding the regulatory effects of quercetin on key pathological processes. We highlight its potential mechanisms of action, including suppression of inflammation and oxidative stress, inhibition of TGF-β1-mediated renal fibrosis, protection of podocyte function, and induction of ferroptosis, and discuss the possible synergistic interactions among these effects in modulating the DN disease network. In addition, we evaluate the current status and limitations of preclinical research on quercetin, and explore feasible strategies-such as nanoparticle-based delivery systems and structural modification-to enhance its bioavailability and tissue targeting. Finally, we propose future research directions for quercetin-based interventions in DN, aiming to provide a theoretical foundation and novel insights for its clinical translation.
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