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The result is a dual-mechanism research tool whose effects can in principle exceed those of either component alone in research models where multiple repair pathways contribute to the outcome
While studies explore plausible mechanisms (NO-system modulation, VEGFR2-Akt-eNOS signaling, GHR/JAK2 in tendon cells), well-controlled human trials are limited
Whether the combination changes the rate is unstudied
It works on a different pathway than either medication, which is why it stacks well with both
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