Abstract：
:In the cardiovascular and hematopoietic systems the Transient Receptor Potential Canonical 3 (TRPC3) channel has a well-recognized role in a number of signaling mechanisms that impact the function of diverse cells and tissues in physiology and disease. The latter includes, but is not limited to, molecular and cellular mechanisms associated to the pathogenesis of cardiac hypertrophy, hypertension and endothelial dysfunction. Despite several of these functions being closely related to atherorelevant mechanisms, the potential roles of TRPC3 in atherosclerosis, the major cause of coronary artery disease, have remained largely unexplored. Over recent years, a series of studies from the authors' laboratory revealed novel functions of TRPC3 in mechanisms related to endothelial inflammation, monocyte adhesion to endothelium and survival and apoptosis of macrophages. The relevance of these new TRPC3 functions to atherogenesis has recently began to receive validation through studies in mouse models of atherosclerosis with conditional gain or loss of TRPC3 function. This chapter summarizes these novel findings and provides a discussion of their impact in the context of atherosclerosis, in an attempt to delineate a framework for further exploration of this terra incognita in the TRPC field.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Vazquez G,Solanki S,Dube P,Smedlund K,Ampem Pdoi
10.1007/978-3-319-26974-0_9subject
Has Abstractpub_date
2016-01-01 00:00:00pages
185-99eissn
0065-2598issn
2214-8019journal_volume
898pub_type
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