No abstract

In addition to decreasing Akt phosphorylation, the results of this study demonstrate, for the first time, the molecular mechanism underlying the effect of IL-6 to decrease the nitric oxide bioavailability by increasing the half-life and, therefore, the protein levels of caveolin-1. The increased caveolin-1 proteins bind more eNOS and consequently decrease eNOS activation by reducing the Ser1177 phosphorylation.

This is a PDF file of an article that has undergone enhancements after acceptance, such as formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, type setting and review before it is published in its final form, but we are providing this version to offer early visibility to the article and its results. Please note that, during the final production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.The original pre-print version of this manuscript was first posted online on March 18 th , 2020. In that version, the authors reported data collected between January 18 th and March 5 th , 2020. Some patients in the cohort were still hospitalized at the time of the original submission. Since that time, the authors have collected additional data reflecting the final disposition of their cohort, and the current pre-print reflects those updated results.

The relationship between hs-CRP and CVsp differed between men and women. Our findings that there is a non-threshold model in men and a threshold model in women provide evidence that more smokers in men (life-style) and age (induction time) contribute to the natural history of CVsp development. The negative effect of hypertension on CVsp suggests that the pathogenesis of CVsp differs from that of coronary atherosclerosis.