ArticleFrontiers in neuroscience2026
Inhibiting the uPAR/FPR1 interactions reduces blood-retinal barrier breakdown and improves retinal function in a rat model of diabetes.
Article in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetic retinopathy (DR) is a leading cause of blindness characterized by early neurovascular damage driven by hyperglycemia-induced mechanisms, including inflammation. The system composed of the urokinase-type plasminogen activator (uPA) and its receptor (uPAR) has previously emerged as a potential regulator of the pro-inflammatory events in DR, possibly through the interaction of uPAR with its lateral partners, such as formyl peptide receptors (FPRs). This study explored whether the inhibition of uPAR/FPR1 crosstalk may reduce early neurovascular alterations in DR by targeting inflammation. To this aim, the new FPR1 antagonist N-19004 was tested in a rat model of streptozotocin-induced diabetes. N-19004 was administered subcutaneously for 7 days at 1 month from diabetes onset. Immunofluorescence, RT-qPCR, Western blot and Evans blue perfusion were performed to evaluate the effects of N-19004 on inflammation, reactive gliosis, blood-retinal barrier (BRB) integrity and apoptosis. In addition, electroretinogram (ERG) was used to assess N-19004 efficacy on retinal function. N-19004 inhibited the activation of inflammation-related transcription factors, including nuclear factor kappa-light-chain-enhancer of activated B cells and signal transducer and activator of transcription 3, leading to reduced interleukin-1β and tumor necrosis factor-
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