Journal
CIRCULATION RESEARCH
Volume 114, Issue 3, Pages 565-571Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.114.300507
Keywords
anoxia; angiogenesis factor; heart failure; hypertrophy; ischemia
Funding
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT)
- Ministry of Health, Labor, and Welfare
- Japan Science and Technology Agency
- Japan Science and Technology Agency, Core Research for Evolutional Science and Technology (CREST)
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [24659390, 23390213] Funding Source: KAKEN
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Cardiac 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.
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