Physiologically assessed hot #flashes and #endothelial function among midlife women.
http://insights.ovid.com/crossref?an=00042192-900000000-97797
Among the younger women, hot flashes explained more variance in flow-mediated dilation than standard cardiovascular disease risk factors or estradiol.
CONCLUSIONS
Among younger midlife women, frequent hot flashes were associated with poorer endothelial function and may provide information about women's vascular status beyond cardiovascular disease risk factors and estradiol.
http://insights.ovid.com/crossref?an=00042192-900000000-97797
Among the younger women, hot flashes explained more variance in flow-mediated dilation than standard cardiovascular disease risk factors or estradiol.
CONCLUSIONS
Among younger midlife women, frequent hot flashes were associated with poorer endothelial function and may provide information about women's vascular status beyond cardiovascular disease risk factors and estradiol.
OvidInsights
Physiologically assessed hot flashes and endothelial function among midlife women.
Hot flashes are experienced by most midlife women. Emerging data indicate that they may be associated with endothelial dysfunction. No studies have tested whether hot flashes are associated with endothelial function using physiologic measures of hot flashes.…
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Reversal of #endothelial dysfunction reduces white #matter vulnerability in cerebral small vessel disease in rats
http://stm.sciencemag.org/content/10/448/eaam9507
One of the most common of dementia in the elderly is cerebral small vessel disease (SVD). Magnetic resonance scans of SVD patients typically show white matter abnormalities, but we do not understand the mechanistic pathological link between blood vessels and white matter myelin damage. Hypertension is suggested as the cause of sporadic SVD, but a recent alternative hypothesis invokes dysfunction of the blood-brain barrier as the primary cause. In a rat model of SVD, we show that endothelial cell (EC) dysfunction is the first change in development of the disease. Dysfunctional ECs secrete heat shock protein 90α, which blocks oligodendroglial differentiation, contributing to impaired myelination. Treatment with EC-stabilizing drugs reversed these EC and oligodendroglial pathologies in the rat model. EC and oligodendroglial dysfunction were also observed in humans with early, asymptomatic SVD pathology. We identified a loss-of-function mutation in ATPase11B, which caused the EC dysfunction in the rat SVD model, and a single-nucleotide polymorphism in ATPase11B that was associated with white matter abnormalities in humans with SVD.
We show that EC dysfunction is a cause of SVD white matter vulnerability and provide a therapeutic strategy to treat and reverse SVD in the rat model, which may also be of relevance to human SVD
Reversal of #endothelial dysfunction reduces white #matter vulnerability in cerebral small vessel disease in rats
http://stm.sciencemag.org/content/10/448/eaam9507
One of the most common of dementia in the elderly is cerebral small vessel disease (SVD). Magnetic resonance scans of SVD patients typically show white matter abnormalities, but we do not understand the mechanistic pathological link between blood vessels and white matter myelin damage. Hypertension is suggested as the cause of sporadic SVD, but a recent alternative hypothesis invokes dysfunction of the blood-brain barrier as the primary cause. In a rat model of SVD, we show that endothelial cell (EC) dysfunction is the first change in development of the disease. Dysfunctional ECs secrete heat shock protein 90α, which blocks oligodendroglial differentiation, contributing to impaired myelination. Treatment with EC-stabilizing drugs reversed these EC and oligodendroglial pathologies in the rat model. EC and oligodendroglial dysfunction were also observed in humans with early, asymptomatic SVD pathology. We identified a loss-of-function mutation in ATPase11B, which caused the EC dysfunction in the rat SVD model, and a single-nucleotide polymorphism in ATPase11B that was associated with white matter abnormalities in humans with SVD.
We show that EC dysfunction is a cause of SVD white matter vulnerability and provide a therapeutic strategy to treat and reverse SVD in the rat model, which may also be of relevance to human SVD
SARS-CoV-2 #Spike Protein Impairs #Endothelial Function via Downregulation of ACE 2
https://2medical.news/2021/05/14/sars-cov-2-spike-protein-impairs-endothelial-function-via-downregulation-of-ace-2/
https://2medical.news/2021/05/14/sars-cov-2-spike-protein-impairs-endothelial-function-via-downregulation-of-ace-2/
2Medical.News
SARS-CoV-2 #Spike Protein Impairs #Endothelial Function via Downregulation of ACE 2
… SARS-CoV-2 infection induces EC inflammation, leading to endotheliitis.1,5 Because S protein decreased ACE2 level and impaired NO bioavailability, we examined whether S protein entry is ind…
Downregulation of Erythrocyte miR-210 Induces #Endothelial Dysfunction in Type 2 #Diabetes
https://2medical.news/2021/11/14/downregulation-of-erythrocyte-mir-210-induces-endothelial-dysfunction-in-type-2-diabetes/
https://2medical.news/2021/11/14/downregulation-of-erythrocyte-mir-210-induces-endothelial-dysfunction-in-type-2-diabetes/
2Medical.News
Downregulation of Erythrocyte miR-210 Induces #Endothelial Dysfunction in Type 2 #Diabetes
Red blood cells (RBCs) act as mediators of vascular injury in type 2 diabetes mellitus (T2DM). miR-210 plays a protective role in cardiovascular homeostasis and is decreased in whole blood of T2DM …