Epigenetic regulation of COL15A1 in smooth muscle cell replicative aging and atherosclerosis.

Smooth muscle cell (SMC) proliferation is a hallmark of vascular injury and disease. Global hypomethylation occurs during SMC proliferation in culture and in vivo during neointimal formation. Regardless of the programmed or stochastic nature of hypomethylation, identifying these changes is important in understanding vascular disease, as maintenance of a cells' epigenetic profile is essential for maintaining cellular phenotype.

Notch activation induces endothelial cell senescence and pro-inflammatory response: implication of Notch signaling in atherosclerosis.

Objective: Notch signaling plays pivotal roles in the pathogenesis of vascular disease. However, little is known about its role in atherosclerosis. We sought to investigate the potential involvement of the Notch signaling in atherosclerosis.

Atherosclerosis, inflammation, genetics, and stem cells: 2012 update.

Atherosclerosis is a peculiar form of inflammation triggered by cholesterol-rich lipoproteins and other noxious factors such as cigarette smoke, diabetes mellitus, and hypertension. Genetics also play an important role in the disease, accounting for about 40% of the risk. Of surprise in recent years of post-human genome sequencing, atherosclerosis-relevant genes discovered by non-biased techniques (ie, genome-wide association studies), did not rehash previously suspected pathways of lipid metabolism, diabetes, or hypertension.

The meaningful use of the review of symptoms in heart failure patients.

Review of symptoms (ROS) is a time-honored tradition in medicine and has proved to be a case-finding maneuver in general medicine patients. The authors sought to investigate the prevalence of noncardiovascular symptoms in heart failure clinics by assessment of the ROS. Of the collected ROS, shortness of breath (SOB) represented the most frequent recalled symptom (8.

Inflammation, stem cells and atherosclerosis genetics.

Atherosclerosis and its associated complications remain the primary cause of death in humans. Aging is the main contributor to atherosclerosis, compared with any other risk factor, yet the specific manner in which age increases risk (the 'aging-risk' mechanism) remains elusive. A novel concept for atherosclerosis risk implicates a lack of endothelial progenitor cell (EPC)-dependent arterial repair in the development of the disease that is secondary to exhaustion of repair-competent EPCs.

Of cardiovascular illness and diversity of biological response.

Noise in gene expression (stochastic variation in the composition of the transcriptome in response to stimuli) may play an important role in maintaining robustness and flexibility, which ensure the stability of normal physiology and provide adaptability to environmental changes for the living system. Broad-based technologies have allowed us to study with unprecedented accuracy the molecular profiles of various states of health and cardiovascular disease. In doing so, we have observed a correlation between the degree of variation in gene expression and the state of health.

Unraveling the genetics of atherosclerosis: implications for diagnosis and treatment.

The hereditary aspect of atherosclerosis has been known for some time in clinical medicine. Over the past three decades, a great deal of research has focused on defining the genetic component of this disease with the hopes that detailed knowledge of the genes and gene variants will lead to improvements in the diagnosis and treatment. This article reviews the different approaches for studying the genetics of atherosclerosis and the potential for using the results in clinical practice.