Proteoglycans are significant modifiers in ischemia and pressure overload-related cardiac remodeling.
Proteoglycans modulate cardiomyocyte hypertrophy, death and proliferation.
Proteoglycans regulate ECM composition and organization to affect cardiac fibrosis.
Proteoglycans take part in inflammatory processes by influencing leukocyte adhesion and migration.
Proteoglycans are promising therapeutic targets in cardiovascular diseases.
Cardiac remodeling is the response of the heart to a range of pathological stimuli. Cardiac remodeling is initially adaptive; however, if sustained, it ultimately causes adverse clinical outcomes. Cardiomyocyte loss or hypertrophy, inflammation and fibrosis are hallmarks of cardiac remodeling. Proteoglycans, which are composed of glycosaminoglycans and a core protein, are a non-structural component of the extracellular matrix. The lack of proteoglycans results in cardiovascular defects during development. Moreover, emerging evidence has indicated that proteoglycans act as significant modifiers in ischemia and pressure overload-related cardiac remodeling. Proteoglycans may also provide novel therapeutic strategies for further improvement in the prognosis of cardiovascular diseases.
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