ArticleJournal of pharmaceutical analysis2025
Naringenin boosts Parkin-mediated mitophagy via estrogen receptor alpha to maintain mitochondrial quality control and heal diabetic foot ulcer.
Article in Journal of pharmaceutical analysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed.
- Dysfunction of mitochondria in intestinal epithelial cells: a key player in the pathogenesis of inflammatory bowel diseases.Gastroenterology report · 2026Review
- Piroxicam accelerates diabetic foot ulcer healing via ERα-dependent mitochondrial protection and oxidative stress relief.Frontiers in pharmacology · 2026Article
- Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic foot ulcer (DFU) is an increasing global burden due to the rising prevalence of diabetes, and no specific pharmacological targets or satisfactory drugs are currently available for this devastating ailment. In this study, naringenin (NAR) was found to accelerate diabetic wound healing in diabetic C57BL/6J wild-type (WT) mice by reducing oxidative stress, as assessed through histological assay. NAR also alleviated the inhibition of proliferation, inflammation, cell senescence, and apoptosis in HaCaT cells induced by high glucose (HG). Mechanistically, the beneficial effects of NAR on wound healing are dependent on the E3 ubiquitin-protein ligase parkin (Parkin/PRKN/Prkn). NAR upregulated the expression level of Parkin and promoted its mitochondrial translocation, thereby activating Parkin-mediated mitophagy and maintaining mitochondrial quality control (MQC). Moreover, the wound healing-promoting effects of NAR were significantly diminished in Parkin knockdown HaCaT cells and
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