Seminars in ophthalmology · 2026
Repurposing Fenofibrate for Early Diabetic Retinopathy: A Systemic and Disease-Modifying Approach.
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Alfaleh Abdulrahman, Al-Kuraishy Hayder M, Alruwaili Mubarak, Eliwa Duaa, Batiha Gaber El-Saber
Аннотация
OBJECTIVE: Diabetic retinopathy (DR) remains a major cause of blindness worldwide, highlighting the need for accessible treatments that prevent its onset and progression. This review explores the potential of repurposing fenofibrate, a traditional lipid-lowering drug, as a systemic, disease-modifying therapy for DR.
METHODS: This narrative synthesis of clinical and molecular studies was conducted to evaluate therapeutic impact of fenofibrate on DR. Evidence from trials was integrated with recent mechanistic data to clarify lipid-independent pathways of fenofibrate in retinal protection.
RESULTS: Fenofibrate significantly reduced the progression of DR independent of serum lipid levels. Mechanistic insights indicate both PPAR-α-dependent and -independent actions that collectively protect retinal microvasculature. These include suppression of inflammation, reduction of oxidative stress, enhancement of endothelial function, and preservation of blood-retinal barrier integrity. The convergence of clinical and molecular evidence suggests that fenofibrate may exert direct retinal benefits beyond its metabolic effects.
CONCLUSIONS: Fenofibrate represents a practical, systemic therapy capable of halting early DR progression. By targeting underlying pathogenic mechanisms, it offers a preventative approach that complements current late-stage ocular interventions and may reduce the global burden of diabetes-related vision loss.
METHODS: This narrative synthesis of clinical and molecular studies was conducted to evaluate therapeutic impact of fenofibrate on DR. Evidence from trials was integrated with recent mechanistic data to clarify lipid-independent pathways of fenofibrate in retinal protection.
RESULTS: Fenofibrate significantly reduced the progression of DR independent of serum lipid levels. Mechanistic insights indicate both PPAR-α-dependent and -independent actions that collectively protect retinal microvasculature. These include suppression of inflammation, reduction of oxidative stress, enhancement of endothelial function, and preservation of blood-retinal barrier integrity. The convergence of clinical and molecular evidence suggests that fenofibrate may exert direct retinal benefits beyond its metabolic effects.
CONCLUSIONS: Fenofibrate represents a practical, systemic therapy capable of halting early DR progression. By targeting underlying pathogenic mechanisms, it offers a preventative approach that complements current late-stage ocular interventions and may reduce the global burden of diabetes-related vision loss.