Genetic variants promoting smooth muscle cell proliferation can result in diffuse and diverse vascular diseases: evidence for a hyperplastic vasculomyopathy.

TL;DR: It is suggested that TIMP4 constitutes a novel therapeutic target for AAA treatment because it is critical in all three aortic aneurysm hallmark processes including degradation of elastin and extracellular matrix protein, loss of medium layer smooth muscle cells, and intense inflammatory cell infiltration.

TL;DR: Three proteome data sets from MNCs are generated using a combination of SDS‐PAGE and nanoflow LC‐MS to build a reference proteome database and identified 514 unique proteins.

TL;DR: The 8th symposium on Marfan syndrome provides a useful summary of the current status of investigations, reveals why life‐expectancy has improved so markedly during the past 30 years, and lays out a clear path for future endeavors.

TL;DR: Clinical and biochemical profiles suggest fibromuscular dysplasia is a systemic disease with altered TGF‐β expression and connective tissue features, and detailed phenotyping of patients with FMD demonstrated that FMD is a systems disease with alterations in common with the spectrum of genetic syndromes that involve altered T GF‐β signaling.

TL;DR: The focus of this review is to provide an overview of the current state of knowledge of molecular mechanisms/processes that control differentiation of vascular smooth muscle cells (SMC) during normal development and maturation of the vasculature, as well as how these mechanisms/ processeses are altered in vascular injury or disease.

TL;DR: Current knowledge of the regulation of SMC differentiation is summarized, with a particular emphasis on consideration of how this process is controlled during normal vascular development and how these control processes might be altered in vascular diseases such as atherosclerosis, which are characterized by marked alterations in the differentiated state of the SMC.