Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 115, Issue 3, Pages 527-537Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200524178
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Funding
- NHLBI NIH HHS [R01 HL059888, R01 HL058010, P01 HL069779, HL58010, HL69779, R01 HL067371, HL61688, P50 HL052319, HL59888, HL67371, HL52319, R01 HL061688] Funding Source: Medline
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In broad terms, there are 3 types of cardiac hypertrophy: normal growth, growth induced by physical conditioning (i.e., physiologic hypertrophy), and growth induced by pathologic stimuli. Recent evidence suggests that normal and exercise-induced cardiac growth are regulated in large part by the growth hormone/IGF axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive cardiac growth is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phospholipase C pathway, leading to an increase in cytosolic calcium and activation of PKC. Here we review recent developments in the area of these cardiotrophic kinases, highlighting the utility of animal models that are helping to identify molecular targets in the human condition.
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