Osteopontin alters endothelial and valvular interstitial cell behaviour in calcific aortic valve stenosis through HMGB1 regulation
Author(s) -
Margaret R. Passmore,
Maria Nataatmadja,
Yoke Lin Fung,
Bronwyn Pearse,
S. Gabriel,
Peter Tesar,
John F. Fraser
Publication year - 2015
Publication title -
european journal of cardio-thoracic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 133
eISSN - 1873-734X
pISSN - 1010-7940
DOI - 10.1093/ejcts/ezv244
Subject(s) - osteopontin , fibrosis , aortic valve , calcification , extracellular matrix , aortic valve stenosis , heart valve , inflammation , hmgb1 , western blot , endothelial stem cell , pathology , medicine , chemistry , biology , microbiology and biotechnology , biochemistry , gene , in vitro
Calcific aortic valve stenosis (CAVS) is an important clinical problem predominantly affecting elderly individuals. Studies suggest that the progression of CAVS is actively regulated with valve endothelial injury leading to inflammation, fibrosis and calcification. The aim of this study was to delineate the possible regulatory role of osteopontin (OPN) on high-mobility group box 1 (HMGB1) function and the associated inflammatory and fibrotic response in CAVS.
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