Abstract

Left ventricular remodeling that occurs after myocardial infarction (MI) and pressure overload is generally accepted as a determinant of the clinical course of heart failure. Mitogen activated protein kinases (MAPK) such as ERK, JNK and p38 appear to be involved in this process. We have attempted to elucidate their roles in the pathogenesis of LV remodeling by analyzing the gene-manipulated mice. Apoptosis signal-regulating kinase 1 (ASK1) is a reactive oxygen species-dependent MAPKKK that plays an important role in stress-induced apoptosis.

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