Growth/differentiation factor 15 (GDF15) was first identified as Macrophage inhibitory cytokine-1 or MIC-1.
It is a protein belonging to the
transforming growth factor beta superfamily. Under normal conditions, GDF-15 is expressed in low concentrations in most organs and upregulated because of injury of organs such as such as liver, kidney, heart and lung.  
The function of GDF-15 is not fully cleared but it seems to have a role in regulating
inflammatory pathways and to be involved in regulating apoptosis, cell repair and cell growth, which are biological processes observed in cardiovascular and neoplastic disorders.   GDF-15 has shown to be a strong prognostic protein in patients with different diseases such as heart diseases and cancer. 
 Metformin was shown to cause increased levels of GDF-15. This increase mediates the effect of body weight loss by metformin.
A monoclonal antibody (mAB1) that neutralizes circulating GDF-15 is being tested in mice and non-human primates as a potential treatment for cancer-related
References [ edit ]
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GRCh38: Ensembl release 89: ENSG00000130513 - Ensembl, May 2017
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GRCm38: Ensembl release 89: ENSMUSG00000038508 - Ensembl, May 2017
"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
Bootcov MR, Bauskin AR, Valenzuela SM, Moore AG, Bansal M, He XY, et al. (October 1997). "MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-beta superfamily". Proceedings of the National Academy of Sciences of the United States of America. 94 (21): 11514–9. Bibcode: 1997PNAS...9411514B. doi: 10.1073/pnas.94.21.11514. PMC . 23523 PMID 9326641.
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Zimmers TA, Jin X, Hsiao EC, McGrath SA, Esquela AF, Koniaris LG (June 2005). "Growth differentiation factor-15/macrophage inhibitory cytokine-1 induction after kidney and lung injury". Shock. 23 (6): 543–8. PMID 15897808.
Hsiao EC, Koniaris LG, Zimmers-Koniaris T, Sebald SM, Huynh TV, Lee SJ (May 2000). "Characterization of growth-differentiation factor 15, a transforming growth factor beta superfamily member induced following liver injury". Molecular and Cellular Biology. 20 (10): 3742–51. doi: 10.1128/MCB.20.10.3742-3751.2000. PMC . 85678 PMID 10779363.
Ago T, Sadoshima J (February 2006). "GDF15, a cardioprotective TGF-beta superfamily protein". Circulation Research. 98 (3): 294–7. doi: . 10.1161/01.RES.0000207919.83894.9d PMID 16484622.
Wollert KC, Kempf T, Lagerqvist B, Lindahl B, Olofsson S, Allhoff T, et al. (October 2007). "Growth differentiation factor 15 for risk stratification and selection of an invasive treatment strategy in non ST-elevation acute coronary syndrome". Circulation. 116 (14): 1540–8. doi: . 10.1161/CIRCULATIONAHA.107.697714 PMID 17848615.
Kempf T, Eden M, Strelau J, Naguib M, Willenbockel C, Tongers J, et al. (February 2006). "The transforming growth factor-beta superfamily member growth-differentiation factor-15 protects the heart from ischemia/reperfusion injury". Circulation Research. 98 (3): 351–60. doi: . 10.1161/01.RES.0000202805.73038.48 PMID 16397141.
Wallentin L, Zethelius B, Berglund L, Eggers KM, Lind L, Lindahl B, et al. (2013). "GDF-15 for prognostication of cardiovascular and cancer morbidity and mortality in men". PLOS ONE. 8 (12): e78797. Bibcode: 2013PLoSO...878797W. doi: 10.1371/journal.pone.0078797. PMC . 3846468 PMID 24312445.
Coll AP, Chen M, Taskar P, Rimmington D, Patel S, Tadross J, et al. (December 2019). "GDF15 mediates the effects of metformin on body weight and energy balance". Nature. 578 (7795): 444–448. doi: 10.1038/s41586-019-1911-y. PMC . 7234839 PMID 31875646.
Wu Z, Bennett D, Brosnan J, Calle RA, Collins S, Esquejo R, et al. (2020). "Growth differentiation factor 15 (GDF-15) neutralization reverses cancer cachexia, restores physical performance and mitigates emesis associated with platinum-based chemotherapy". Annals of Oncology. 31 (suppl_4): S245–S259. doi: 10.1016/annonc/annonc265 (inactive 2021-01-14). CS1 maint: DOI inactive as of January 2021 ( link)
External links [ edit ]