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doi: 10.1073/pnas.82.23.8232 111 ProchaskaH

Accordingly, be cautious

In animal models, it has been shown preclinically to upregulate growth hormone receptors in tendon fibroblasts, stimulate angiogenesis via the VEGFR2/Akt-eNOS pathway, and modulate nitric oxide signaling, mechanisms that, if they translate to humans, could support tissue repair in a hormonal environment where estrogen-dependent healing capacity is declining

Correcting the measurement does not automatically alter the underlying disease process

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