ArticleAndrology2025
Therapeutic potential of hesperidin in diabetes mellitus-induced erectile dysfunction through Nrf2-mediated ferroptosis and oxidative stress.
Article in Andrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Hesperidin mitigates cognitive and anxiety-like deficits by enhancing hippocampal antioxidant defenses, reducing neuroinflammation, and preventing neuronal apoptosis in a third-trimester-equivalent rat model of developmental ethanol neurotoxicity.IBRO neuroscience reports · 2026Article
- Male testosterone synthesis disorders: oxidative stress pathways, regulatory mechanisms, potential of antioxidant therapy, and botanical medicine prospects.Asian journal of andrology · 2026Review
- Hesperidin from Chenpi Ameliorates Skin Photoaging by Targeting HSPA1L to Stabilize GPX4 and Suppress Ferroptosis.Antioxidants (Basel, Switzerland) · 2026Article
- From symptomatic relief to restorative medicine: a comprehensive review of diabetic erectile dysfunction.Translational andrology and urology · 2026Review
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Exploring the application of shear stress in erectile dysfunction.Asian journal of andrology · 2026Review
- Quercetin alleviates radiation-induced erectile dysfunction by modulating oxidative stress and apoptosis through the Nrf2/HO-1 pathway.European journal of medical research · 2026Article
- Mechanisms of dyslipidemia-induced erectile dysfunction: a narrative review.Frontiers in endocrinology · 2026Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Therapeutic potential of hesperidin in diabetes mellitus-induced erectile dysfunction through Nrf2-mediated ferroptosis and oxidative stress.Andrology · 2025Article
- The role of programmed cell death in diabetes mellitus-induced erectile dysfunction: from mechanisms to targeted therapy.Reproductive biology and endocrinology : RB&E · 2025Review
- Current status and advances in adipose-derived stem cells therapy for diabetes mellitus erectile dysfunction.Frontiers in medicine · 2025Review
- A Novel Flavonoid Derivative of Icariside II (YS-10) Improves Erectile Dysfunction in a Diabetic Rat Model by Inhibiting Ferroptosis via Activation of the Nrf2/HO-1/GPX4 Pathway.Drug design, development and therapy · 2025Article
- Metabolic Syndrome-Associated Erectile Dysfunction: Multiple Vascular Endothelial Dysfunction Mechanisms and Potential Therapeutic Targets.International journal of biological sciences · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
backgroundAmong erectile dysfunction (ED) caused by metabolic abnormalities, diabetes mellitus-induced ED (DMED) progresses rapidly, manifests with severe symptoms, and shows reduced responsiveness to conventional medications. Hyperglycemia in the corpus cavernosum has been linked to the induction of both ferroptosis and oxidative stress, which are mediated by nuclear factor E2 related factor 2 (Nrf2). Hesperidin (Hes), a flavonoid compound, has been revealed to activate Nrf2 in certain diabetic complications, yet the efficacy of Hes on DMED and the specific mechanism remain unclear.
objectivesTo elucidate the potential mechanism and efficacy of Hes in regulating Nrf2-mediated ferroptosis and oxidative stress in DMED. MATERIALS AND
methodsDMED rats were constructed through the intraperitoneal injection of streptozotocin (STZ), partially supplemented with Hes. In parallel, in vitro research utilized human umbilical vein endothelial cells (HUVECs), with glucose addition to simulating a high glucose (HG) environment, and induced with Hes or ML385 (an Nrf2 inhibitor). Penile tissues and HUVECs were harvested for subsequent analyses.
resultsThe results of this study indicate that Hes partially reversed the impaired erectile function. The expression of Nrf2, glutathione peroxidase 4 (GPX4), and heme oxygenase-1 (HO-1) in the corpus cavernosum elevated after supplementing with Hes, resulted in an inhibition in ferroptosis and oxidative stress. Moreover, the quantity and function of erectile effector cells were restored, and cavernous fibrosis was ameliorated. In HG-induced HUVECs, Hes ameliorated Nrf2-mediated ferroptosis and oxidative stress, effects which ML385 partially reversed.
conclusionsHes exerts a therapeutic effect on DMED rats and a regulatory mechanism on the Nrf2-HO-1/GPX4 axis, concurrently revitalizing endothelial and smooth muscle cells, and diminishing fibrosis. Our study provides robust preclinical evidence for employing Hes in treating DMED.
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