Abstract
The heart has been recognized as an endocrine organ for over 30 years (de Bold, 2011); however, little is known about how the heart communicates with other organs in the body, and even less is known about this process in the diseased heart. In this issue of EMBO Molecular Medicine, Magida and Leinwand (2014) introduce the concept that a primary genetic defect in the heart results in aberrant hepatic lipid metabolism, which consequently exacerbates hypertrophic cardiomyopathy (HCM). This study provides evidence in support of the hypothesis that crosstalk occurs between the heart and liver, and that this becomes disrupted in the diseased state.
Highlights
The heart has been recognized as an endocrine organ for over 30 years; little is known about how the heart communicates with other organs in the body, and even less is known about this process in the diseased heart
Mutations in MYH7 increase force generation and actin-myosin sliding velocity within sarcomeres. These findings indicate that genetic mutations in hypertrophic cardiomyopathy (HCM) patients are the primary cause of cardiac hypertrophy (Wang et al, 2010)
Numerous animal models have been generated to investigate HCM (Maass & Leinwand, 2000), and much focus has been given to an R403Q mutation in MYH7, which causes an especially severe clinical phenotype (Seidman & Seidman, 2011)
Summary
The heart has been recognized as an endocrine organ for over 30 years (de Bold, 2011); little is known about how the heart communicates with other organs in the body, and even less is known about this process in the diseased heart. These findings indicate that genetic mutations in HCM patients are the primary cause of cardiac hypertrophy (Wang et al, 2010). Numerous animal models have been generated to investigate HCM (Maass & Leinwand, 2000), and much focus has been given to an R403Q mutation in MYH7, which causes an especially severe clinical phenotype (Seidman & Seidman, 2011).
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