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AuthorSuleiman, Muna
AuthorAbdurrahman, Nabeel
Authoryalcin, huseyin c
AuthorMraiche, Fatima
Available date2018-08-15T04:42:46Z
Publication Date2018-08-01
Publication NameLife Sciences
Identifierhttp://dx.doi.org/10.1016/j.lfs.2018.08.009
CitationSuleiman, M., Abdulrahman, N., Yalcin, H., & Mraiche, F. (2018). The role of CD44, hyaluronan and NHE1 in cardiac remodeling. Life sciences.
ISSN0024-3205
URIhttp://hdl.handle.net/10576/6828
AbstractCardiac remodeling, characterized by excessive extracellular matrix (ECM) remodeling, predisposes the heart to failure if left unresolved. Understanding the signaling mechanisms involved in excessive extracellular matrix (ECM) remodeling is necessary to identify the means to regress the development of cardiac remodeling and heart failure. Recently, hyaluronan (HA), a ubiquitously expressed glycosaminoglycan in the ECM, was shown to participate in tissue fibrosis and myofibroblast proliferation through interacting with its ubiquitously expressed cell-surface receptor, CD44. CD44 is a multifunctional transmembrane glycoprotein that serves as a cell-surface receptor for a number of ECM proteins. The mechanism by which the interaction between CD44-HA contributes to ECM and cardiac remodeling remains unknown. A previous study performed on a non-cardiac model showed that CD44-HA enhances Na/H exchanger isoform-1 (NHE-1) activity, causing ECM remodeling, HA metabolism and tumor invasion. Interestingly, NHE-1 has been demonstrated to be involved in cardiac remodeling and myocardial fibrosis. In addition, it has previously been demonstrated that CD44 is upregulated in transgenic mouse hearts expressing active NHE-1. The role of CD44, HA and NHE1 and the cellular interplay of these factors in the ECM and cardiac remodeling is the focus of this review.
Languageen
PublisherElsevier
Subjectcardiac remodeling
cardiac hypertrophy
extracellular matrix remodeling
heart failure
cardiac fibroblast
CD44
Hyaluranon
NHE-1
Fibrsosis
TitleThe role of CD44, hyaluronan and NHE1 in cardiac remodeling.
TypeArticle
Pagination197-201
Volume Number209
ESSN1879-0631
dc.accessType Abstract Only


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