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      Metabolic Crosstalk between the Heart and Fat

      review-article
      , MS, , PhD
      Korean Circulation Journal
      The Korean Society of Cardiology
      Cardiac myocytes, Adipocytes, Crosstalk, Adipokines, Cardiokines

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          Abstract

          It is now recognized that the heart can behave as a true endocrine organ, which can modulate the function of other tissues. Emerging evidence has shown that visceral fat is one such distant organ the heart communicates with. In fact, it appears that bi-directional crosstalk between adipose tissue and the myocardium is crucial to maintenance of normal function in both organs. In particular, factors secreted from the heart are now known to influence the metabolic activity of adipose tissue and other organs, as well as modulate the release of metabolic substrates and signaling molecules from the periphery. This review summarizes current knowledge regarding primary cardiokines and adipokines involved in heart-fat crosstalk, as well as implications of their dysregulation for cardiovascular health.

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          Most cited references73

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          Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis.

          Gradients of signalling and transcription factors govern many aspects of embryogenesis, highlighting the need for spatiotemporal control of regulatory protein levels. MicroRNAs are phylogenetically conserved small RNAs that regulate the translation of target messenger RNAs, providing a mechanism for protein dose regulation. Here we show that microRNA-1-1 (miR-1-1) and miR-1-2 are specifically expressed in cardiac and skeletal muscle precursor cells. We found that the miR-1 genes are direct transcriptional targets of muscle differentiation regulators including serum response factor, MyoD and Mef2. Correspondingly, excess miR-1 in the developing heart leads to a decreased pool of proliferating ventricular cardiomyocytes. Using a new algorithm for microRNA target identification that incorporates features of RNA structure and target accessibility, we show that Hand2, a transcription factor that promotes ventricular cardiomyocyte expansion, is a target of miR-1. This work suggests that miR-1 genes titrate the effects of critical cardiac regulatory proteins to control the balance between differentiation and proliferation during cardiogenesis.
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            Peroxisome proliferator-activated receptor gamma coactivator-1 promotes cardiac mitochondrial biogenesis.

            Cardiac mitochondrial function is altered in a variety of inherited and acquired cardiovascular diseases. Recent studies have identified the transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) as a regulator of mitochondrial function in tissues specialized for thermogenesis, such as brown adipose. We sought to determine whether PGC-1 controlled mitochondrial biogenesis and energy-producing capacity in the heart, a tissue specialized for high-capacity ATP production. We found that PGC-1 gene expression is induced in the mouse heart after birth and in response to short-term fasting, conditions known to increase cardiac mitochondrial energy production. Forced expression of PGC-1 in cardiac myocytes in culture induced the expression of nuclear and mitochondrial genes involved in multiple mitochondrial energy-transduction/energy-production pathways, increased cellular mitochondrial number, and stimulated coupled respiration. Cardiac-specific overexpression of PGC-1 in transgenic mice resulted in uncontrolled mitochondrial proliferation in cardiac myocytes leading to loss of sarcomeric structure and a dilated cardiomyopathy. These results identify PGC-1 as a critical regulatory molecule in the control of cardiac mitochondrial number and function in response to energy demands.
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              MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice.

              MicroRNAs (miRNAs) are a class of small noncoding RNAs that have gained status as important regulators of gene expression. Here, we investigated the function and molecular mechanisms of the miR-208 family of miRNAs in adult mouse heart physiology. We found that miR-208a, which is encoded within an intron of alpha-cardiac muscle myosin heavy chain gene (Myh6), was actually a member of a miRNA family that also included miR-208b, which was determined to be encoded within an intron of beta-cardiac muscle myosin heavy chain gene (Myh7). These miRNAs were differentially expressed in the mouse heart, paralleling the expression of their host genes. Transgenic overexpression of miR-208a in the heart was sufficient to induce hypertrophic growth in mice, which resulted in pronounced repression of the miR-208 regulatory targets thyroid hormone-associated protein 1 and myostatin, 2 negative regulators of muscle growth and hypertrophy. Studies of the miR-208a Tg mice indicated that miR-208a expression was sufficient to induce arrhythmias. Furthermore, analysis of mice lacking miR-208a indicated that miR-208a was required for proper cardiac conduction and expression of the cardiac transcription factors homeodomain-only protein and GATA4 and the gap junction protein connexin 40. Together, our studies uncover what we believe are novel miRNA-dependent mechanisms that modulate cardiac hypertrophy and electrical conduction.
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                Author and article information

                Journal
                Korean Circ J
                Korean Circ J
                KCJ
                Korean Circulation Journal
                The Korean Society of Cardiology
                1738-5520
                1738-5555
                May 2020
                22 January 2020
                : 50
                : 5
                : 379-394
                Affiliations
                Center for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
                Author notes
                Correspondence to Walter J. Koch, PhD. Center for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, 3500 N Broad Street, Philadelphia, PA 19140, USA. walter.koch@ 123456temple.edu
                Author information
                https://orcid.org/0000-0001-9711-7683
                https://orcid.org/0000-0002-0609-8649
                Article
                10.4070/kcj.2019.0400
                7098822
                32096362
                0f889cb5-f9ec-428c-9eb2-9775d479ce83
                Copyright © 2020. The Korean Society of Cardiology

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( https://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted noncommercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 10 December 2019
                : 27 December 2019
                Funding
                Funded by: American Heart Association, CrossRef https://doi.org/10.13039/100000968;
                Award ID: AMERIT33900036
                Categories
                Review Article

                Cardiovascular Medicine
                cardiac myocytes,adipocytes,crosstalk,adipokines,cardiokines
                Cardiovascular Medicine
                cardiac myocytes, adipocytes, crosstalk, adipokines, cardiokines

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