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      Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart

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          Abstract

          The post-natal heart adapts to stress and overload through hypertrophic growth, a process that may be pathologic or beneficial (physiologic hypertrophy). Physiologic hypertrophy improves cardiac performance in both healthy and diseased individuals, yet the mechanisms that propagate this favorable adaptation remain poorly defined. We identify the cytokine cardiotrophin 1 (CT1) as a factor capable of recapitulating the key features of physiologic growth of the heart including transient and reversible hypertrophy of the myocardium, and stimulation of cardiomyocyte-derived angiogenic signals leading to increased vascularity. The capacity of CT1 to induce physiologic hypertrophy originates from a CK2-mediated restraining of caspase activation, preventing the transition to unrestrained pathologic growth. Exogenous CT1 protein delivery attenuated pathology and restored contractile function in a severe model of right heart failure, suggesting a novel treatment option for this intractable cardiac disease.

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          Most cited references 72

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          2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.

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            Programmed cell death in animal development and disease.

            Programmed cell death (PCD) plays a fundamental role in animal development and tissue homeostasis. Abnormal regulation of this process is associated with a wide variety of human diseases, including immunological and developmental disorders, neurodegeneration, and cancer. Here, we provide a brief historical overview of the field and reflect on the regulation, roles, and modes of PCD during animal development. We also discuss the function and regulation of apoptotic proteins, including caspases, the key executioners of apoptosis, and review the nonlethal functions of these proteins in diverse developmental processes, such as cell differentiation and tissue remodeling. Finally, we explore a growing body of work about the connections between apoptosis, stem cells, and cancer, focusing on how apoptotic cells release a variety of signals to communicate with their cellular environment, including factors that promote cell division, tissue regeneration, and wound healing. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Cardiac plasticity.

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                Author and article information

                Affiliations
                [1 ]Sprott Centre for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa Hospital , Ottawa, Ontario K1H 8L6, Canada
                [2 ]Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa , Ottawa, Ontario K1H 8M5, Canada
                [3 ]University of Ottawa Heart Institute , Ottawa, Ontario K1Y 4W7, Canada
                [4 ]Department of Biology, Carleton University , Ottawa, Ontario K1S 5B6, Canada
                [5 ]Fate Therapeutics Inc. , 3535 General Atomics Court Suite 200, San Diego, CA 92121, USA
                [6 ]Department of Medicine (Cardiology), Faculty of Medicine, University of Ottawa , Ottawa, Ontario K1H 8M5, Canada
                Author notes
                [✝]

                These two authors contributed equally to this work.

                Journal
                Cell Res
                Cell Res
                Cell Research
                Nature Publishing Group
                1001-0602
                1748-7838
                October 2017
                08 August 2017
                1 October 2017
                : 27
                : 10
                : 1195-1215
                28785017 5630684 cr201787 10.1038/cr.2017.87
                Copyright © 2017 The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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