The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure
Oncostatin M (OSM), a member of the interleukin-6 family, functions as a major mediator of cardiomyocyte remodeling under pathological conditions. Its involvement in a variety of human cardiac diseases such as aortic stenosis, myocardial infarction, myocarditis, cardiac sarcoidosis, and various card...
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| Format: | Article |
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MDPI AG
2022-02-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/3/1811 |
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| author | Thomas Kubin Praveen Gajawada Peter Bramlage Stefan Hein Benedikt Berge Ayse Cetinkaya Heiko Burger Markus Schönburg Wolfgang Schaper Yeong-Hoon Choi Manfred Richter |
| author_facet | Thomas Kubin Praveen Gajawada Peter Bramlage Stefan Hein Benedikt Berge Ayse Cetinkaya Heiko Burger Markus Schönburg Wolfgang Schaper Yeong-Hoon Choi Manfred Richter |
| author_sort | Thomas Kubin |
| collection | DOAJ |
| description | Oncostatin M (OSM), a member of the interleukin-6 family, functions as a major mediator of cardiomyocyte remodeling under pathological conditions. Its involvement in a variety of human cardiac diseases such as aortic stenosis, myocardial infarction, myocarditis, cardiac sarcoidosis, and various cardiomyopathies make the OSM receptor (OSMR) signaling cascades a promising therapeutic target. However, the development of pharmacological treatment strategies is highly challenging for many reasons. In mouse models of heart disease, OSM elicits opposing effects via activation of the type II receptor complex (OSMR/gp130). Short-term activation of OSMR/gp130 protects the heart after acute injury, whereas chronic activation promotes the development of heart failure. Furthermore, OSM has the ability to integrate signals from unrelated receptors that enhance fetal remodeling (dedifferentiation) of adult cardiomyocytes. Because OSM strongly stimulates the production and secretion of extracellular proteins, it is likely to exert systemic effects, which in turn, could influence cardiac remodeling. Compared with the mouse, the complexity of OSM signaling is even greater in humans because this cytokine also activates the type I leukemia inhibitory factor receptor complex (LIFR/gp130). In this article, we provide an overview of OSM-induced cardiomyocyte remodeling and discuss the consequences of OSMR/gp130 and LIFR/gp130 activation under acute and chronic conditions. |
| first_indexed | 2024-03-09T23:43:27Z |
| format | Article |
| id | doaj.art-05e72667d9864005a1df775bf5cd0c83 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T23:43:27Z |
| publishDate | 2022-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-05e72667d9864005a1df775bf5cd0c832023-11-23T16:47:00ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-02-01233181110.3390/ijms23031811The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and FailureThomas Kubin0Praveen Gajawada1Peter Bramlage2Stefan Hein3Benedikt Berge4Ayse Cetinkaya5Heiko Burger6Markus Schönburg7Wolfgang Schaper8Yeong-Hoon Choi9Manfred Richter10Department of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyInstitute for Pharmacology and Preventive Medicine GmbH, Bahnhofstraße 20, 49661 Cloppenburg, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyMax-Planck-Institute for Heart and Lung Research, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyDepartment of Cardiac Surgery, Kerckhoff Heart Center, Benekestr. 2-8, 61231 Bad Nauheim, GermanyOncostatin M (OSM), a member of the interleukin-6 family, functions as a major mediator of cardiomyocyte remodeling under pathological conditions. Its involvement in a variety of human cardiac diseases such as aortic stenosis, myocardial infarction, myocarditis, cardiac sarcoidosis, and various cardiomyopathies make the OSM receptor (OSMR) signaling cascades a promising therapeutic target. However, the development of pharmacological treatment strategies is highly challenging for many reasons. In mouse models of heart disease, OSM elicits opposing effects via activation of the type II receptor complex (OSMR/gp130). Short-term activation of OSMR/gp130 protects the heart after acute injury, whereas chronic activation promotes the development of heart failure. Furthermore, OSM has the ability to integrate signals from unrelated receptors that enhance fetal remodeling (dedifferentiation) of adult cardiomyocytes. Because OSM strongly stimulates the production and secretion of extracellular proteins, it is likely to exert systemic effects, which in turn, could influence cardiac remodeling. Compared with the mouse, the complexity of OSM signaling is even greater in humans because this cytokine also activates the type I leukemia inhibitory factor receptor complex (LIFR/gp130). In this article, we provide an overview of OSM-induced cardiomyocyte remodeling and discuss the consequences of OSMR/gp130 and LIFR/gp130 activation under acute and chronic conditions.https://www.mdpi.com/1422-0067/23/3/1811oncostatin M receptorleukemia inhibitory factor receptorgp130interleukin-6cardiomyocyteinflammation |
| spellingShingle | Thomas Kubin Praveen Gajawada Peter Bramlage Stefan Hein Benedikt Berge Ayse Cetinkaya Heiko Burger Markus Schönburg Wolfgang Schaper Yeong-Hoon Choi Manfred Richter The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure International Journal of Molecular Sciences oncostatin M receptor leukemia inhibitory factor receptor gp130 interleukin-6 cardiomyocyte inflammation |
| title | The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure |
| title_full | The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure |
| title_fullStr | The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure |
| title_full_unstemmed | The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure |
| title_short | The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure |
| title_sort | role of oncostatin m and its receptor complexes in cardiomyocyte protection regeneration and failure |
| topic | oncostatin M receptor leukemia inhibitory factor receptor gp130 interleukin-6 cardiomyocyte inflammation |
| url | https://www.mdpi.com/1422-0067/23/3/1811 |
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