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Atherosclerosis and platelets

Soluble guanylyl cyclase in platelets keeps atherosclerosis at bay

The contribution of platelets to atherothrombosis is well established. Accumulating genome-wide association studies have revealed several variants of genes encoding molecules along the nitric oxide (NO)–soluble guanylyl cyclase (sGC)–cyclic guanosine-3′,5′-monophosphate (cGMP) pathway that are associated with increased risk of coronary artery disease; however, the cell types and functional impact of these risk variants remain poorly understood. Mauersberger et al. now demonstrate that platelet-specific knockout of a transcript encoding sGC increased atherosclerosis, whereas pharmacological stimulators of sGC reduced lesions via a paracrine effect of angiopoietin-1 on endothelial cell–leukocyte interactions.

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Fig. 1: Atheroprotective effects of the non-risk sGC allele.


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Supported by the US National Institutes of Health (HL115141, HL134849, HL148207, HL148355, HL153356 to M.W.F.) and the American Heart Association (18SFRN33900144 and 20SFRN35200163 to M.W.F.).

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Correspondence to Mark W. Feinberg.

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Jamaiyar, A., Chen, J. & Feinberg, M.W. Soluble guanylyl cyclase in platelets keeps atherosclerosis at bay. Nat Cardiovasc Res 1, 1124–1126 (2022).

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