Endothelial mechanosensing: A forgotten target to treat vascular remodeling in hypertension?

The endothelium is a mechanosensitive organ whose pleiotropic actions regulate vessel structure to adjust tissue perfusion. To do so, it possesses ion channels, receptor complexes, and signaling pathways responding to blood flow, whose activation will either maintain vascular integrity and quiescence or, on the contrary, remodel the vessel's structure in both health and disease. Recent studies have demonstrated the crucial role of endothelial inflammation, endothelial to mesenchymal transition (EndMT), and perturbed hemodynamics in the progression of pulmonary arterial hypertension and essential hypertension. These two distinct diseases share some common mechanistic cues, pointing towards new potential therapeutic approaches to treat them. In this review, we summarize these common mechanisms to map future drug development strategies targeting flow sensing mechanisms and vascular remodeling.

SP-D and CC-16 Pneumoproteins' Kinetics and Their Predictive Role During SARS-CoV-2 Infection.

BACKGROUND: Surfactant protein D (SP-D) and pulmonary club cell protein 16 (CC-16) are called "pneumoproteins" and are involved in host defense against oxidative stress, inflammation, and viral outbreak. This study aimed to determine the predictive value of these pneumoproteins on the incidence of acute respiratory distress syndrome (ARDS) or death in patients with coronavirus disease-2019 (COVID-19). METHODS: This retrospective study included 87 patients admitted to an emergency department. Blood samples were collected on three time points (days 1, 5, and 14 from hospital admission). SP-D and CC-16 serum levels were determined, and univariate and multivariate analyses considering confounding variables (age, body mass index, tobacco use, dyspnea, hypertension, diabetes mellitus, neutrophil-to-lymphocyte ratio) were performed. RESULTS: Based on the multivariate analysis, SP-D level on D1 was positively and slightly correlated with subsequent development of ARDS, independent of body mass index, dyspnea, and diabetes mellitus. CC-16 level on D1 was modestly and positively correlated with fatal outcome. A rise in SP-D between D1 and D5 and D1 and D14 had a strong negative association with incidence of ARDS. These associations were independent of tobacco use and neutrophil-to-lymphocyte ratio. CONCLUSIONS: Overall, our data reveal that increase in SP-D levels is a good prognostic factor for patients with COVID-19, and that initial CC-16 levels correlated with slightly higher risk of death. SP-D and CC-16 may prove useful to predict outcomes in patients with COVID-19.