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TRPV1 is a non-GPCR ion channel that directly binds LPA (18:1) at its C-terminal Lys710 residue (K 0 ≈754 nM), leading to channel opening and pain behavior independent of G proteins (60)

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There's no strong theoretical reason to weight angiogenesis more heavily than cell migration (or vice versa) in tissue-repair research — both are prerequisites for repair, both contribute distinct mechanisms, and neither obviously dominates the other in published research models