• Toru Oka, Hiroshi Akazawa, Atsuhiko T Naito, and Issei Komuro.
• From the Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan (T.O., A.T.N., I.K.); Departments of Advanced Clinical Science and Therapeutics (H.A.) and Cardiovascular Medicine (H.A., A.T.N., I.K.), The University of Tokyo Graduate School of Medicine, Bunkyo-ku, Tokyo, Japan; and Japan Science and Technology Agency, Core Research for Evolutional Science and Technology (CREST), Chiyoda-ku, Tokyo, Japan (T.O., H.A., A.T.N., I.K.).
• Circ. Res. 2014 Jan 31; 114 (3): 565-71.

AbstractCardiac hypertrophy is an adaptive response to physiological and pathological overload. In response to the overload, individual cardiac myocytes become mechanically stretched and activate intracellular hypertrophic signaling pathways to re-use embryonic transcription factors and to increase the synthesis of various proteins, such as structural and contractile proteins. These hypertrophic responses increase oxygen demand and promote myocardial angiogenesis to dissolve the hypoxic situation and to maintain cardiac contractile function; thus, these responses suggest crosstalk between cardiac myocytes and microvasculature. However, sustained pathological overload induces maladaptation and cardiac remodeling, resulting in heart failure. In recent years, specific understanding has increased with regard to the molecular processes and cell-cell interactions that coordinate myocardial growth and angiogenesis. In this review, we summarize recent advances in understanding the regulatory mechanisms of coordinated myocardial growth and angiogenesis in the pathophysiology of cardiac hypertrophy and heart failure.

24 keywords...

hide…