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      The Role of Cardiokines in Heart Diseases: Beneficial or Detrimental?

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      Author(s): 1 , 2 , 3 , 1 , , 3 ,
      Publication date (Electronic):
      Journal: BioMed Research International
      Publisher: Hindawi

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          Abstract

          Cardiovascular disease remains the leading cause of morbidity and mortality, imposing a major disease burden worldwide. Therefore, there is an urgent need to identify new therapeutic targets. Recently, the concept that the heart acts as a secretory organ has attracted increasing attention. Proteins secreted by the heart are called cardiokines, and they play a critical physiological role in maintaining heart homeostasis or responding to myocardial damage and thereby influence the development of heart diseases. Given the critical role of cardiokines in heart disease, they might represent a promising therapeutic target. This review will focus on several cardiokines and discuss their roles in the pathogenesis of heart diseases and as potential therapeutics.

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          Most cited references121

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          ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Update the 2001 Guidelines for the Evaluation and Management of Heart Failure): developed in collaboration with the American College of Chest Physicians and the International Society for Heart and Lung Transplantation: endorsed by the Heart Rhythm Society.

          Sharon Ann Hunt, William T. Abraham, Marshall Chin … (2005)
          Article 0 comments Cited 313 times – based on 0 reviews     Review now
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            Epicardial FSTL1 reconstitution regenerates the adult mammalian heart.

            Ke Wei, Vahid Serpooshan, Cecilia Hurtado … (2015)
            The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans.
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              Expression and regulation of ST2, an interleukin-1 receptor family member, in cardiomyocytes and myocardial infarction.

              S Tominaga, Ellen Weinberg, M Shimpo … (2002)
              We identified an interleukin-1 receptor family member, ST2, as a gene markedly induced by mechanical strain in cardiac myocytes and hypothesized that ST2 participates in the acute myocardial response to stress and injury. ST2 mRNA was induced in cardiac myocytes by mechanical strain (4.7+/-0.9-fold) and interleukin-1beta (2.0+/-0.2-fold). Promoter analysis revealed that the proximal and not the distal promoter of ST2 is responsible for transcriptional activation in cardiac myocytes by strain and interleukin-1beta. In mice subjected to coronary artery ligation, serum ST2 was transiently increased compared with unoperated controls (20.8+/-4.4 versus 0.8+/-0.8 ng/mL, P<0.05). Soluble ST2 levels were increased in the serum of human patients (N=69) 1 day after myocardial infarction and correlated positively with creatine kinase (r=0.41, P<0.001) and negatively with ejection fraction (P=0.02). These data identify ST2 release in response to myocardial infarction and suggest a role for this innate immune receptor in myocardial injury.
              Article 0 comments Cited 170 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ling Yang:
                ORCID: http://orcid.org/0000-0002-7885-3287
                Chun Yang:
                ORCID: http://orcid.org/0000-0003-1540-4385
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2018
                Publication date (Electronic): 18 March 2018
                Volume: 2018
                Electronic Location Identifier: 8207058
                Affiliations
                1Department of Cardiology, The Third Affiliated Hospital of Soochow University, Changzhou 213003, China
                2Department of Critical Care Medicine, The Third Affiliated Hospital of Soochow University, Changzhou 213003, China
                3Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China
                Author notes

                Academic Editor: Rei Shibata

                Author information
                http://orcid.org/0000-0002-7885-3287
                http://orcid.org/0000-0003-1540-4385
                Article
                DOI: 10.1155/2018/8207058
                PMC ID: 5878913
                PubMed ID: 29744364
                SO-VID: 0d1a2171-33bd-4176-ad5b-0359bd146659
                Copyright © Copyright © 2018 Ye-Shun Wu et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 30 November 2017
                Date revision received : 19 January 2018
                Date accepted : 7 February 2018
                Funding
                Funded by: Program of Bureau of Science and Technology Foundation of Changzhou
                Award ID: CJ20159022
                Award ID: CJ20160030
                Funded by: Changzhou Municipal Committee of Health and Family Planning
                Award ID: ZD201505
                Award ID: ZD201407
                Categories
                Subject: Review Article

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