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Growth Differentiation Factor 15 in Heart Failure: An Update

  • Pathophysiology of Myocardial Failure (IS Anand, Section Editor)
  • Published:
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Abstract

Growth differentiation factor 15 (GDF-15) is a stress-responsive cytokine expressed in the cardiovascular system. GDF-15 is emerging as a biomarker of cardiometabolic risk and disease burden. GDF-15 integrates information from cardiac and extracardiac disease pathways that are linked to the incidence, progression, and prognosis of heart failure (HF). Increased circulating levels of GDF-15 are associated with an increased risk of developing HF in apparently healthy individuals from the community. After an acute coronary syndrome, elevated levels of GDF-15 are indicative of an increased risk of developing adverse left ventricular remodeling and HF. In patients with established HF, the levels of GDF-15 and increases in GDF-15 over time are associated with adverse outcomes. The information provided by GDF-15 is independent of established risk factors and cardiac biomarkers, including BNP. More studies are needed to elucidate how the information provided by GDF-15 can be used for patient monitoring and formulating treatment decisions. Further understanding of the pathobiology of GDF-15 may lead to the discovery of new treatment targets in HF.

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Acknowledgement

K. C. Wollert is supported by grants from the Germany Research Foundation (DFG), the Germany Ministry of Education and Research (BMBF), and Roche Diagnostics.

Disclosure

K. C. Wollert has received compensation from Roche Diagnostics for serving as a consultant and for lectures, including service on speakers’ bureaus. T. Kempf has received compensation from Roche Diagnostics for providing expert testimony. Both authors are named as coinventors on a patent for the use of GDF-15 for cardiovascular applications and have a contract with Roche Diagnostics for the development of a GDF-15 assay.

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Wollert, K.C., Kempf, T. Growth Differentiation Factor 15 in Heart Failure: An Update. Curr Heart Fail Rep 9, 337–345 (2012). https://doi.org/10.1007/s11897-012-0113-9

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