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From the previous evidence, in dyslipidemia-related ED, angiogenesis is disrupted due to (1) endothelial NOS downregulation and NO depletion, (2) superoxide-mediated NO degradation, and (3) oxidized low-density lipoprotein/lysophosphatidylcholine-induced inhibition of endothelial migrationkey processes driven by arterial wall atherogenesis [127]

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Anything that can artificially accelerate healing or modify biological processes at a fundamental level is going to attract intense scrutiny