Plasma NEDD9 is increased following SARS‐CoV‐2 infection and associates with indices of pulmonary vascular dysfunction

Alba, George A.; Zhou, Iris Y.; Mascia, Molly; Magaletta, Michael; Alladina, Jehan W.; Giacona, Francesca L.; Ginns, Leo C.; Caravan, Peter; Maron, Bradley A.; Montesi, Sydney B.

doi:10.1002/pul2.12356

Cited by 1 publication

(1 citation statement)

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“…Regarding the pulmonary vascular bed, Zhou et al demonstrated reduced pulmonary microvascular perfusion in 10 COVID-19 patients (8 months after infection) compared to age-matched healthy volunteers using dynamic performed contrast-enhanced magnetic resonance imaging (DCE-MRI) [139]. Interestingly, as in PAH [140], increased plasmatic levels of the prothrombotic protein NEDD9 have been described in these patients, reflecting pulmonary endothelial dysfunction [141].…”

Section: Persistent Vascular Endothelial Dysfunctionmentioning

confidence: 99%

Mechanisms of Pulmonary Vasculopathy in Acute and Long-Term COVID-19: A Review

Riou,

Coste,

Meyer

et al. 2024

IJMS

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Despite the end of the pandemic, coronavirus disease 2019 (COVID-19) remains a major public health concern. The first waves of the virus led to a better understanding of its pathogenesis, highlighting the fact that there is a specific pulmonary vascular disorder. Indeed, COVID-19 may predispose patients to thrombotic disease in both venous and arterial circulation, and many cases of severe acute pulmonary embolism have been reported. The demonstrated presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) within the endothelial cells suggests that direct viral effects, in addition to indirect effects of perivascular inflammation and coagulopathy, may contribute to pulmonary vasculopathy in COVID-19. In this review, we discuss the pathological mechanisms leading to pulmonary vascular damage during acute infection, which appear to be mainly related to thromboembolic events, an impaired coagulation cascade, micro- and macrovascular thrombosis, endotheliitis and hypoxic pulmonary vasoconstriction. As many patients develop post-COVID symptoms, including dyspnea, we also discuss the hypothesis of pulmonary vascular damage and pulmonary hypertension as a sequela of the infection, which may be involved in the pathophysiology of long COVID.

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Section: Persistent Vascular Endothelial Dysfunctionmentioning

confidence: 99%