Jeffrey kubes
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Specimens were analyzed for lipid, collagen, macrophage, lymphocyte, neutrophil, mast cell and smooth muscle cell content, and chemokine and cytokine mRNA expression. Methods-Regions upstream and downstream the blood flow were isolated from internal carotid plaques of patients asymptomatic (n63) or symptomatic (n18) for ischemic stroke. Thus, we investigated the possible role of systemic and intraplaque inflammation in patients asymptomatic versus symptomatic for ischemic stroke. 2010 107:1304-1312.) Key Words: fibroblasts fibrosis fate mapping Physiological cardiac function and chronic heart failure arecontrolled by complex interactions of the myocytes, extracellular matrix (ECM), and nonmyocyte cellular compo-nents, including the cardiac fibroblasts.1,2 With their various functions, cardiac fibroblasts are at the interface of multiple interactions, playing an integral part in maintaining ho-meostasis in the heart.3,4 Under physiological conditions, cardiac fibroblasts contribute to the structural, mechanical,īackground and Purpose-The concept of “vulnerable plaque ” has been extended to the more recent definition of the “cardiovascular vulnerable patient, ” in which “intraplaque ” and “systemic ” factors contribute to the cumulative risk of acute cardiovascular events. Here, we review our emerging understanding of where cardiac fibroblasts come from, as well as how we can possibly use this knowledge to develop novel therapies for cardiac fibrosis. Evidence is evolving that cardiac fibroblasts are a heterogeneous population and likely derive from various distinct tissue niches in health and disease. Despite their manyfold functions, cardiac fibroblasts remain poorly character-ized in molecular terms. They are indispens-able for damage control and tissue remodeling on myocardial injury and principal mediators of pathological cardiac remodeling and fibrosis.
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Abstract: Cardiac fibroblasts play a critical role in maintenance of normal cardiac function.