How Estrogen Controls Cardiac Hypertrophy

Cardiac hypertrophy has been found to occur in nearly 80% of heart attack patients.

Investigators at the University of California, Irvine (USA), worked with cultured rat cardiomyocytes (heart cells). They reported in the July 15, 2005, issue of the Journal of Biological Chemistry that treatment of the cells with the estrogen 17 beta-estradiol (E2) significantly prevented angiotensin II (AngII)- or endothelin-1 (ET-1)-induced new protein synthesis, skeletal muscle actin expression, and increased surface area. E2 prevented ET-1 from stimulating calcineurin phosphatase activity, which normally results in new protein synthesis. E2 induced the MCIP1 gene, an inhibitor of AngII-induced calcineurin activity, via phosphatidylinositol 3-kinase, transcriptional, and mRNA stability mechanisms. Small interfering RNA for MCIP1 significantly reversed both the E2's ability to suppress protein synthesis and its inhibition of calcineurin activity.

"There has been intense reaction to the Women's Health Initiative report indicating that estrogen is not beneficial in preventing coronary heart disease,” said senior author Dr. Ellis R. Levin, professor of medicine, biochemistry, and pharmacology at the University of California, Irvine. "Our work suggests that further in-depth studies should be undertaken to determine if estrogen supplements prevent cardiac hypertrophy, especially in postmenopausal women with risk factors for this disorder. Existing research results in women support this concept.”