Short communication

Elevation of plasma oncostatin M in heart failure

*Author for correspondence:

E-mail Address: damien.gruson@uclouvain.be

Pôle de recherche en Endocrinologie, Diabète et Nutrition, Institut de Recherche Expérimentale et Clinique, Cliniques Universitaires St-Luc & Université Catholique de Louvain, Brussels, Belgium

Department of Laboratory Medicine, Cliniques Universitaires St-Luc & Université Catholique de Louvain, Brussels, Belgium

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Benjamin Ferracin

Department of Laboratory Medicine, Cliniques Universitaires St-Luc & Université Catholique de Louvain, Brussels, Belgium

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Sylvie A Ahn

Division of Cardiology, Cliniques Universitaires St-Luc & Pôle de recherche cardiovasculaire, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Brussels, Belgium

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Michel F Rousseau

Division of Cardiology, Cliniques Universitaires St-Luc & Pôle de recherche cardiovasculaire, Institut de Recherche Expérimentale et Clinique, Université Catholique de Louvain, Brussels, Belgium

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Published Online:6 Jun 2017https://doi.org/10.2217/fca-2016-0063

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Abstract

Aim: Oncostatin M (OSM) is an inflammatory cytokine of the gp130 family. OSM could participate in adverse cardiovascular remodeling through regulation of FGF23. Materials & methods: OSM levels were determined in 80 heart failure patients with reduced left ventricular ejection fraction (HFrEF). Results: OSM levels are significantly increased in HFrEF patients compared with healthy subjects. We have also demonstrated that, in HFrEF patients, plasma OSM levels are correlated to parathyroid hormone PTH(1–84) and 1,25(OH)₂D, two other biomarkers related to bone and mineral metabolism and associated to adverse cardiovascular outcomes. Conclusion: OSM concentrations are elevated in HFrEF patients and could interplay with parathyroid hormone and vitamin D impacting cardiovascular function. Nevertheless, the prognostic value of OSM testing appears limited.

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References

1 Ponikowski P, Voors AA, Anker SD et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur. J. Heart Fail. 37(27), 2129–2200 (2016).Google Scholar
2 Andersen IA, Huntley BK, Sandberg SS, Heublein DM, Burnett JC Jr. Elevation of circulating but not myocardial FGF23 in human acute decompensated heart failure. Nephrol. Dial. Transplant. 31(5), 767–772 (2016).Crossref, Medline, CAS, Google Scholar
3 Wang TJ, Pencina MJ, Booth SL et al. Vitamin D deficiency and risk of cardiovascular disease. Circulation 117(4), 503–511 (2008).Crossref, Medline, CAS, Google Scholar
4 Scialla JJ, Wolf M. Roles of phosphate and fibroblast growth factor 23 in cardiovascular disease. Nat. Rev. Nephrol. 10(5), 268–278 (2014).Crossref, Medline, CAS, Google Scholar
5 Touchberry CD, Green TM, Tchikrizov V et al. FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy. Am. J. Physiol. Endocrinol. Metab. 304(8), E863–E873 (2013).Crossref, Medline, CAS, Google Scholar
6 Gruson D, Buglioni A, Burnett JC Jr. PTH: potential role in management of heart failure. Clin. Chim. Acta 433, 290–296 (2014).Crossref, Medline, CAS, Google Scholar
7 Tunon J, Cristobal C, Tarin N et al. Coexistence of low vitamin D and high fibroblast growth factor-23 plasma levels predicts an adverse outcome in patients with coronary artery disease. PLoS ONE 9(4), e95402 (2014).Crossref, Medline, Google Scholar
8 Schierbeck LL, Jensen TS, Bang U, Jensen G, Kober L, Jensen JE. Parathyroid hormone and vitamin D-markers for cardiovascular and all cause mortality in heart failure. Eur. J. Heart Fail. 13(6), 626–632 (2011).Crossref, Medline, CAS, Google Scholar
9 Silver J, Rodriguez M, Slatopolsky E. FGF23 and PTH – double agents at the heart of CKD. Nephrol. Dial. Transplant. 27(5), 1715–1720 (2012).Crossref, Medline, CAS, Google Scholar
10 Udell JA, Morrow DA, Jarolim P et al. Fibroblast growth factor-23, cardiovascular prognosis, and benefit of angiotensin-converting enzyme inhibition in stable ischemic heart disease. J. Am. Coll. Cardiol. 63(22), 2421–2428 (2014).Crossref, Medline, CAS, Google Scholar
11 Gutierrez OM, Januzzi JL, Isakova T et al. Fibroblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease. Circulation 119(19), 2545–2552 (2009).Crossref, Medline, CAS, Google Scholar
12 Mirza MA, Larsson A, Melhus H, Lind L, Larsson TE. Serum intact FGF23 associate with left ventricular mass, hypertrophy and geometry in an elderly population. Atherosclerosis 207(2), 546–551 (2009).Crossref, Medline, CAS, Google Scholar
13 Richter M, Lautze HJ, Walther T, Braun T, Kostin S, Kubin T. The failing heart is a major source of circulating FGF23 via oncostatin M receptor activation. J. Heart Lung Transplant 34(9), 1211–1214 (2015).Crossref, Medline, Google Scholar
14 Richards CD. The enigmatic cytokine oncostatin m and roles in disease. ISRN Inflamm. 512103 (2013).Medline, Google Scholar
15 Sims NA, Quinn JMW. Osteoimmunology: oncostatin M as a pleiotropic regulator of bone formation and resorption in health and disease. Bonekey Rep. 3, 527 (2014).Crossref, Medline, CAS, Google Scholar
16 Seiler S, Reichart B, Roth D, Seibert E, Fliser D, Heine GH. FGF-23 and future cardiovascular events in patients with chronic kidney disease before initiation of dialysis treatment. Nephrol. Dial. Transplant 25(12), 3983–3989 (2010).Crossref, Medline, CAS, Google Scholar
17 Gruson D, Lepoutre T, Ketelslegers JM, Cumps J, Ahn SA, Rousseau MF. C-terminal FGF23 is a strong predictor of survival in systolic heart failure. Peptides 37(2), 258–262 (2012).Crossref, Medline, CAS, Google Scholar
18 Kubin T, Poling J, Kostin S et al. Oncostatin is a major mediator of cardiomyocyte dedifferentiation and remodeling. Cell Stem Cell 9(5), 420–432 (2011).Crossref, Medline, CAS, Google Scholar
19 Zhang X, Zhu D, Wei L et al. OSM enhances angiogenesis and improves cardiac function after myocardial infarction. Biomed. Res. Int. 317905 (2015).Medline, Google Scholar
20 Li X, Zhang X, Wei L, Xia Y, Guo X. Relationship between serum oncostatin M levels and degree of coronary stenosis in patients with coronary artery disease. Clin. Lab. 60(1), 113–118 (2014).Medline, CAS, Google Scholar
21 Sanchez-Infantes D, White UA, Elks CM et al. Oncostatin m is produced in adipose tissue and is regulated in conditions of obesity and Type 2 diabetes. J. Clin. Endocrinol. Metab. 99(2), E217–E225 (2014).Crossref, Medline, CAS, Google Scholar
22 Komori T, Tanaka M, Furuta H, Akamizu T, Miyajima A, Morikawa Y. Oncostatin M is a potential agent for the treatment of obesity and related metabolic disorders: a study in mice. Diabetologia. 58(8), 1868–1876 (2015).Crossref, Medline, CAS, Google Scholar
23 Poling J, Gajawada P, Richter M et al. Therapeutic targeting of the oncostatin M receptor-beta prevents inflammatory heart failure. Basic Res. Cardiol. 109(1), 396 (2014).Crossref, Medline, Google Scholar

Vol. 13, No. 3

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Published online 6 June 2017

Published in print May 2017

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Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Ethical conduct of research

The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations. In addition, for investigations involving human subjects, informed consent has been obtained from the participants involved.

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