Discover the pivotal role of PFKFB3 in neovascular eye diseases and how unraveling its mechanisms opens doors to innovative therapeutic strategies.
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PFKFB3 in neovascular eye disease: unraveling mechanisms and exploring therapeutic strategies.
Liu et al., Cell Biosci 2024
<!– DOI: 10.1186/s13578-024-01205-9 //–>
https://doi.org/10.1186/s13578-024-01205-9
Neovascular eye diseases like proliferative diabetic retinopathy (PDR), age-related macular degeneration (AMD), and retinopathy of prematurity (ROP) lead to blindness due to abnormal blood vessel growth. While anti-VEGF therapies have been central to treatment, they have limitations and side effects. Emerging therapies focusing on metabolism, specifically targeting the enzyme PFKFB3, show promise in offering an alternative or adjunct to anti-VEGF treatments.
This review highlights the mechanisms of neovascular eye diseases and the potential of PFKFB3 as a therapeutic target. It discusses the enzyme’s role, the effects of its inhibitors, and the future of PFKFB3-targeted treatments. The importance of this information lies in the potential for PFKFB3 inhibitors to provide new treatment avenues for patients with poor prognosis under anti-VEGF therapy and to reduce long-term side effects of VEGF inhibitors.
The review suggests that targeting PFKFB3-mediated glycolysis could be a significant step forward in treating neovascular eye diseases, with several drugs already advancing into clinical research stages.