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Conversely, the overexpression of Erv1 led to a higher OxD at steady state in the IMS (Supplementary Figure S8)

Prior research indicates that exogenous NO not only inhibits platelet aggregation and leukocyte adhesion and diminishes the inflammatory response, but also activates guanylate cyclase and enhances the synthesis of cyclic guanosine monophosphate, which induces myosin dephosphorylation in vascular smooth muscle and ultimately facilitates vascular smooth muscle relaxation and augments organ perfusion and energy reserves (7880)

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