Robert S Ross1. 1. Department of Physiology, and The Cardiovascular Research Laboratories, David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, CA 90095, USA.
Abstract
BACKGROUND: Integrins are a large family of heterodimeric cell surface receptors that are present on all cells. These molecules link the extracellular matrix to the intracellular cytoskeleton and are multifunctional, playing roles in cell organization and differentiation, migration, alteration of gene expression, and cell survival. They signal bidirectionally across the cell membrane. Most interestingly from the cardiovascular viewpoint, they have been shown to function as mechanotransducers. METHODS: Although a great deal of studies have been performed that document the biologic function of integrins in a general sense, only recently have data shown their role in the heart. The repertoire of integrins present on cells is modulated in the remodeled myocardium. Further, hemodynamic loading may alter key integrin-mediated signaling events. Perturbation of integrin function in the heart of intact animals has documented the importance of these molecules in the myocardium. CONCLUSION: Future work is required to gain additional information on the role of integrins in the normal and pathologic heart so that we can evaluate if integrins expressed on the cardiac myocyte should be considered as a therapeutic target during cardiac remodeling.
BACKGROUND: Integrins are a large family of heterodimeric cell surface receptors that are present on all cells. These molecules link the extracellular matrix to the intracellular cytoskeleton and are multifunctional, playing roles in cell organization and differentiation, migration, alteration of gene expression, and cell survival. They signal bidirectionally across the cell membrane. Most interestingly from the cardiovascular viewpoint, they have been shown to function as mechanotransducers. METHODS: Although a great deal of studies have been performed that document the biologic function of integrins in a general sense, only recently have data shown their role in the heart. The repertoire of integrins present on cells is modulated in the remodeled myocardium. Further, hemodynamic loading may alter key integrin-mediated signaling events. Perturbation of integrin function in the heart of intact animals has documented the importance of these molecules in the myocardium. CONCLUSION: Future work is required to gain additional information on the role of integrins in the normal and pathologic heart so that we can evaluate if integrins expressed on the cardiac myocyte should be considered as a therapeutic target during cardiac remodeling.
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