Quercetin and Nephrotoxicity: A Narrative Review of Cellular Pathways and Therapeutic Possibilities

Zahra Yazdanpanah1, Hossein Sobhani1,2, Mahboobeh Navabi1,2

  • 1School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.

Insights

Quercetin, a natural flavonoid, shows significant potential in protecting kidneys from damage caused by toxins and treatments. It combats oxidative stress, inflammation, and cell death, offering a promising therapeutic strategy for nephrotoxicity.

Area of Science:

  • Nephrology
  • Pharmacology
  • Biochemistry

Background:

  • Nephrotoxicity poses a significant clinical challenge, often resulting from chemotherapy, environmental factors, and metabolic issues.
  • Current treatments for kidney damage lack effective molecular protection, highlighting the need for new therapeutic approaches.
  • Quercetin, a plant-derived flavonoid, exhibits notable nephroprotective effects attributed to its antioxidant, anti-inflammatory, and anti-apoptotic properties.

Purpose of the Study:

  • To review and synthesize recent research (2021-2025) on quercetin's therapeutic role in preventing and mitigating kidney toxicity.
  • To explore the molecular mechanisms underlying quercetin's nephroprotective actions.
  • To assess quercetin's potential as an adjunctive therapy for nephrotoxicity.

Main Methods:

  • Comprehensive literature search of PubMed, Scopus, Web of Science, and Google Scholar.
  • Inclusion of in vitro, in vivo, and clinical studies published between 2021 and 2025.
  • Analysis of studies investigating quercetin's impact on renal function markers, oxidative stress, inflammation, apoptosis, and autophagy.

Main Results:

  • Quercetin improves renal function by reducing serum creatinine and urea, and restoring antioxidant enzymes (SOD, CAT, GPx).
  • It modulates key signaling pathways, including Sirt1/Nrf2/HO-1, NF-κB, MAPK/ERK, and AKT1, to maintain redox balance and promote cell survival.
  • Quercetin effectively suppresses inflammation, regulates apoptosis (Bax/Bcl-2, caspase), and enhances autophagy (Beclin 1, LC3β, TFEB), preserving renal structure and reducing fibrosis.

Conclusions:

  • Quercetin provides multi-targeted nephroprotection through integrated antioxidant, anti-inflammatory, anti-apoptotic, and autophagic mechanisms.
  • Its ability to modulate critical signaling pathways makes it a strong candidate for adjunctive nephroprotective therapy.
  • Further research is warranted to optimize quercetin's bioavailability, evaluate long-term safety, and explore its clinical applications.

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