Dynamic cell-cell and cell-ECM interactions in the heart

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• 作者：Catherine M. Howard^a ; Troy A. Baudino^b ; ^c ; ^{tbaudino@medicine.tamhsc.edu" class="auth_mail}
• 关键词：Cardiac fibroblasts ; Myocytes ; Cell&ndash ; cell interactions ; Extracellular matrix ; Cardiac remodeling
• 刊名：Journal of Molecular and Cellular Cardiology
• 出版年：May, 2014
• 年：2014
• 卷：70
• 期：Complete
• 页码：19-26
• 全文大小：718 K

文摘

Recent studies have placed an increasing amount of emphasis on the cardiovascular system and understanding how the heart and its vasculature can be regenerated following pathological stresses, such as hypertension and myocardial infarction. The remodeling process involves the permanent cellular constituents of the heart including myocytes, fibroblasts, endothelial cells, pericytes, smooth muscle cells and stem cells. It also includes transient cell populations, such as immune cells (e.g. lymphocytes, mast cells and macrophages) and circulating stem cells. Following injury, there are dramatic shifts in the various cardiac cell populations that can affect cell-cell and cell-extracellular matrix interactions and cardiac function. Cardiac fibroblasts are a key component in normal heart function, as well as during the remodeling process through dynamic cell-cell interactions and synthesis and degradation of the extracellular matrix. Fibroblasts dynamically interact with the various cardiac cell populations through mechanical, chemical (autocrine and/or paracrine) and electrophysiological means to alter gene and protein expression, cellular processes and ultimately cardiac function. Better understanding these cell-cell and cell-extracellular matrix interactions and their biological consequences should provide novel therapeutic targets for the treatment of heart disease. In this review we discuss the nature of these interactions and the importance of these interactions in maintaining normal heart function, as well as their role in the cardiac remodeling process. This article is part of a Special Issue entitled "Myocyte-Fibroblast Signalling in Myocardium."