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Mechanisms matter, but so does methodological discipline

Proposed mechanisms include upregulation of growth-hormone-receptor expression in injured tissue, VEGF-driven angiogenesis, modulation of the nitric-oxide pathway in vascular endothelium, and activation of FAK-paxillin signaling

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What underpins progression at the tissue, cellular and molecular levels is still unknown, but taken together, emerging data strongly point to an underlying chronic cytodegenerative process starting early and operating largely independently of overt inflammation

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