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Vascular endothelial growth factor receptor 1 (FLT1) mRNA is the transcript encoding the FLT1 protein, a high-affinity tyrosine kinase receptor for VEGF-A, VEGF-B, and placental growth factor (PlGF) (NCBI Gene ID: 2321). A key feature of this target is the production of a soluble isoform, sFlt-1, through alternative splicing of the mRNA, which acts as a potent antagonist to pro-angiogenic signaling by sequestering circulating ligands (UniProt: P17948). In diseases such as preeclampsia, the over-expression of sFlt-1 mRNA in the placenta leads to excessive protein secretion, causing systemic endothelial damage and hypertension in the mother (Turanov et al., 2018). Therapeutic strategies targeting FLT1 mRNA utilize RNA interference (RNAi) or antisense oligonucleotides to selectively reduce the levels of these transcripts, particularly the soluble variant, to restore vascular homeostasis (Brownfoot et al., 2016). This approach is currently being explored as a precision medicine strategy to treat pregnancy-related complications and various angiogenic disorders where protein-level inhibition is desired (Zeisler et al., 2016).
RNA interference (RNAi) or antisense-mediated degradation of mRNA to inhibit protein translation
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