Protection and reversal of hepatic fibrosis by red wine polyphenols in hyperhomocysteinemic mice.

Hyperhomocysteinemia leads to several clinical manifestations and, particularly, liver disease. Lowering homocysteine through nutrition or other means might offer preventive or therapeutic benefits. Polyphenols are natural compounds known for their antioxidant and healing properties for vessels.

Myocardial fibrosis and TGFB expression in hyperhomocysteinemic rats.

Hyperhomocysteinemia, characterized by an elevated plasma homocysteine concentration, leads to several clinical manifestations and particularly cardiovascular diseases. Experimental models of hyperhomocysteinemia revealed several tissue injuries including heart fibrosis and ventricular hypertrophy. In order to analyze the molecular mechanisms link to these morphological alterations, a mild hyperhomocysteinemia was induced in rats via a chronic methionine administration.

Hyperhomocysteinemia-induced Dyrk1a downregulation results in cardiomyocyte hypertrophy in rats.

Cardiac hypertrophy has been demonstrated in rat models of hyperhomocysteinemia, a major risk factor for chronic heart failure. As one of the molecular pathway which leads to cardiac hypertrophy is mediated by the serine-threonine kinase DYRK1A, we have determined the expression of Dyrk1a in the heart of hyperhomocysteinemic rats and found that hyperhomocysteinemia in rats not only induced ventricular cardiomyocyte hypertrophy but also decreased protein Dyrk1a expression. The decreased expression of Dyrk1a could be consistent with decreased antihypertrophic effects of Dyrk1a leading to cardiomyocyte hypertrophy in case of hyperhomocysteinemia.