Abstract
The Workshop on Cardiovascular Extracellular Matrix in Health and Disease, International University of Andalusia, Baeza, Spain, 6-8 October 2014 served to discuss the current knowledge on the mechanisms integral to extracellular matrix homeostasis that are fundamental to understanding the pathological basis of several cardiovascular diseases, including the development of cardiac fibrosis in response to cardiac hypertrophy and myocardial infarction, and the extracellular matrix alterations contributing to aortic stenosis or aneurysms.
Highlights
Distinguishable from the glycocalix, the membranebound, carbohydrate-rich cell coat, the extracellular matrix (ECM) constitutes the organic matter found between most cells in plants and animals
The Workshop on Cardiovascular Extracellular Matrix in Health and Disease, International University of Andalusia, Baeza, Spain, 6-8 October 2014 served to discuss the current knowledge on the mechanisms integral to extracellular matrix homeostasis that are fundamental to understanding the pathological basis of several cardiovascular diseases, including the development of cardiac fibrosis in response to cardiac hypertrophy and myocardial infarction, and the extracellular matrix alterations contributing to aortic stenosis or aneurysms
The meeting aimed to bring together top-level, highly experienced investigators working on different aspects of cardiovascular ECM pathophysiology and mechanisms of fibrosis initiation, propagation, and regression in an attempt to shed
Summary
Distinguishable from the glycocalix, the membranebound, carbohydrate-rich cell coat, the extracellular matrix (ECM) constitutes the organic matter found between most cells in plants and animals. The Workshop on Cardiovascular Extracellular Matrix in Health and Disease, International University of Andalusia, Baeza, Spain, 6-8 October 2014 served to discuss the current knowledge on the mechanisms integral to extracellular matrix homeostasis that are fundamental to understanding the pathological basis of several cardiovascular diseases, including the development of cardiac fibrosis in response to cardiac hypertrophy and myocardial infarction, and the extracellular matrix alterations contributing to aortic stenosis or aneurysms.
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