Matricellular Proteins: New Molecular Targets To Prevent Heart Failure
被引:47
作者:
Okamoto, Hiroshi
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机构:
Hokkaido Med Ctr, Dept Cardiovasc Med, Nishi Ku, Sapporo, Hokkaido 0630005, JapanHokkaido Med Ctr, Dept Cardiovasc Med, Nishi Ku, Sapporo, Hokkaido 0630005, Japan
Okamoto, Hiroshi
[1
]
Imanaka-Yoshida, Kyoko
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机构:
Mie Univ, Grad Sch Med, Dept Pathol & Matrix Biol, Tsu, Mie 514, Japan
Mie Univ, Res Ctr Matrix Biol, Tsu, Mie 514, JapanHokkaido Med Ctr, Dept Cardiovasc Med, Nishi Ku, Sapporo, Hokkaido 0630005, Japan
Imanaka-Yoshida, Kyoko
[2
,3
]
机构:
[1] Hokkaido Med Ctr, Dept Cardiovasc Med, Nishi Ku, Sapporo, Hokkaido 0630005, Japan
[2] Mie Univ, Grad Sch Med, Dept Pathol & Matrix Biol, Tsu, Mie 514, Japan
[3] Mie Univ, Res Ctr Matrix Biol, Tsu, Mie 514, Japan
Matricellular proteins are highly expressed in reparative responses to pressure and volume overload, ischemia, oxidative stress after myocardial injury, and modulate the inflammatory and fibrotic process in ventricular remodeling, which leads to cardiac dysfunction and eventually overt heart failure. Generally, matricellular proteins loosen strong adhesion of cardiomyocytes to extracellular matrix, which would help cells to move for rearrangement and allow inflammatory cells and capillary vessels to spread during tissue remodeling. Among matricellular proteins, osteopontin (OPN) and tenascin-C (TN-C) are de-adhesion proteins and upregulate the expression and activity of matrix metalloproteinases. These matricellular proteins could be key molecules to diagnose cardiac remodeling and also might be targets for the prevention of adverse ventricular remodeling. This review provides an overview of the role of matricellular proteins such as OPN and TN-C in cardiac function and remodeling, as determined by both in basic and in clinical studies.