Atherosclerosis is a chronic progressive inflammatory process that can eventually lead to cardiovascular disease (CVD). Despite available treatment, the prevalence of atherosclerotic CVD, which has become the leading cause of death worldwide, persists. Identification of new mechanisms of atherogenesis are highly needed in order to develop an effective therapeutic treatment. The blood vessels contain two primary major cell types: endothelial cells (EC) and vascular smooth muscle cells (VSMC). Each of these performs an essential function in sustaining vascular homeostasis. EC-VSMC communication is essential not only to development, but also to the homeostasis of mature blood vessels. Aberrant EC-VSMC interaction could promote atherogenesis. Identification of the mode of EC-VSMC crosstalk that regulates vascular functionality and sustains homeostasis may offer strategic insights for prevention and treatment of atherosclerotic CVD. Here we will review the molecular mechanisms underlying the interplay between EC and VSMC that could contribute to atherosclerosis. We also highlight open questions for future research directions.
Although the construct validity of the 7-factor model of the PDSS was not supported for this sample of mothers, additional factor analytic work was used to develop and provide initial validation of a 5-factor model. Future research should continue to explore the unique experiences of mothers in the NICU who experience postpartum depression.
Obesity has a strong impact on the pathogenesis of cardiovascular disease, which raises enthusiasm to understand how excess adiposity causes vascular injury. Adipose tissue is an essential regulator of cardiovascular system through its endocrine and paracrine bioactive products. Obesity induces endothelial dysfunction, which often precedes and leads to the development of cardiovascular diseases. Connecting adipose tissue-endothelial cell interplay to endothelial dysfunction may help us to better understand obesity-induced cardiovascular disease. This Mini Review discussed (1) the general interactions and obesity-induced endothelial dysfunction, (2) potential targets, and (3) the outstanding questions for future research.
Alcohol consumption during pregnancy can produce adverse outcomes; maternal smoking compounds this risk. We examined prevalence of smoking and associations between smoking and alcohol use in Russian women of childbearing age (N = 648). Smoking was reported by 35% of nonpregnant and 14% of pregnant women. Smoking prevalence was higher (45%) among at-risk drinkers and those at risk for an alcohol-exposed pregnancy (AEP). In a multivariate model, smoking status and city of residence significantly predicted AEP risk. Pregnant women in urban locations were more likely to smoke. Smoking and alcohol misuse often co-occur among Russian women, presenting risk for dual prenatal exposure.
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