ArticleIn vivo (Athens, Greece)
Study on the Role of Short Peptide LCKLSL Targeting ANXA2 in Retinal Neovascularization.
Article in In vivo (Athens, Greece). 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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3 authors.
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Abstract
BACKGROUND/
aimAnnexin A2 (ANXA2), functioning as a co-receptor for tissue plasminogen activator (tPA) and plasminogen, plays a critical role in retinal neovascularization (RNV). The hexapeptide LCKLSL competitively inhibits ANXA2 activity, offering a potential therapeutic strategy for RNV in retinopathy of prematurity (ROP). This study investigated the efficacy and biosafety of LCKLSL in suppressing RNV using an oxygen-induced retinopathy (OIR) model in C57BL/6J mice. MATERIALS AND
methodsLCKLSL was administered
resultsLCKLSL significantly attenuated RNV formation without inducing pathological alterations in retinal structure or systemic toxicity. Mechanistically, LCKLSL reduced cell-surface tPA binding and suppressed vascular endothelial growth factor (VEGF) and metalloproteinase (MMP) expression at mRNA and protein levels.
conclusionLCKLSL acts as a potent ANXA2-targeted inhibitor of pathological angiogenesis and demonstrates a favorable biosafety profile, highlighting its promising therapeutic potential for the treatment of RNV-related disorder.
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