GDF15 and Growth Control

doi:10.3389/fphys.2018.01712

Review

. 2018 Nov 27:9:1712.

doi: 10.3389/fphys.2018.01712. eCollection 2018.

GDF15 and Growth Control

Paul J Emmerson¹, Kevin L Duffin¹, Sudhakar Chintharlapalli¹, Xinle Wu²

Affiliations

¹ Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN, United States.
² Lilly China Innovation and Partnerships, Shanghai, China.

PMID: 30542297
PMCID: PMC6277789
DOI: 10.3389/fphys.2018.01712

Review

GDF15 and Growth Control

Paul J Emmerson et al. Front Physiol. 2018.

. 2018 Nov 27:9:1712.

doi: 10.3389/fphys.2018.01712. eCollection 2018.

Authors

Paul J Emmerson¹, Kevin L Duffin¹, Sudhakar Chintharlapalli¹, Xinle Wu²

Affiliations

¹ Lilly Research Laboratories, Eli Lilly and Company, Indianapolis, IN, United States.
² Lilly China Innovation and Partnerships, Shanghai, China.

PMID: 30542297
PMCID: PMC6277789
DOI: 10.3389/fphys.2018.01712

Abstract

Growth/differentiation factor-15 (GDF-15) is a distant member of the transforming growth factor β (TGF-β) superfamily and is widely expressed in multiple mammalian tissues. Its expression is highly regulated and is often induced in response to conditions associated with cellular stress. GDF15 serum levels have a strong association with many diseases, including inflammation, cancer, cardiovascular diseases, and obesity, and potentially serve as reliable predictor of disease progression. A functional role for GDF15 has been suggested in cancer, cardiovascular disease, kidney disease and metabolic disease. However, the knowledge of its pathophysiological function at the molecular level is still limited and requires more investigation. Recent identification of the endogenous receptor for GDF15 may provide additional insight in to its' molecular mechanisms and relationship to disease states.

Keywords: GDF15; GFRAL; TGFβ; cancer; cardiovascular; metabolic; obesity.

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References

1. Adela R., Banerjee S. K. (2015). GDF-15 as a target and biomarker for diabetes and cardiovascular diseases: a translational prospective. J. Diabetes Res. 2015:490842. 10.1155/2015/490842 - DOI - PMC - PubMed
1. Airaksinen M. S., Saarma M. (2002). The GDNF family: signalling, biological functions and therapeutic value. Nat. Rev. Neurosci. 3 383–394. 10.1038/nrn812 - DOI - PubMed
1. Albertoni M., Shaw P. H., Nozaki M., Godard S., Tenan M., Hamou M. F., et al. (2002). Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1. Oncogene 21 4212–4219. 10.1038/sj.onc.1205610 - DOI - PubMed
1. Artz A., Butz S., Vestweber D. (2016). GDF-15 inhibits integrin activation and mouse neutrophil recruitment through the ALK-5/TGF-betaRII heterodimer. Blood 128 529–541. 10.1182/blood-2016-01-696617 - DOI - PubMed
1. Baek S. J., Kim K. S., Nixon J. B., Wilson L. C., Eling T. E. (2001). Cyclooxygenase inhibitors regulate the expression of a TGF-beta superfamily member that has proapoptotic and antitumorigenic activities. Mol. Pharmacol. 59 901–908. 10.1124/mol.59.4.901 - DOI - PubMed

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[1] Adela R., Banerjee S. K. (2015). GDF-15 as a target and biomarker for diabetes and cardiovascular diseases: a translational prospective. J. Diabetes Res. 2015:490842. 10.1155/2015/490842 - DOI - PMC - PubMed

[2] Adela R., Banerjee S. K. (2015). GDF-15 as a target and biomarker for diabetes and cardiovascular diseases: a translational prospective. J. Diabetes Res. 2015:490842. 10.1155/2015/490842 - DOI - PMC - PubMed

[3] Airaksinen M. S., Saarma M. (2002). The GDNF family: signalling, biological functions and therapeutic value. Nat. Rev. Neurosci. 3 383–394. 10.1038/nrn812 - DOI - PubMed

[4] Airaksinen M. S., Saarma M. (2002). The GDNF family: signalling, biological functions and therapeutic value. Nat. Rev. Neurosci. 3 383–394. 10.1038/nrn812 - DOI - PubMed

[5] Albertoni M., Shaw P. H., Nozaki M., Godard S., Tenan M., Hamou M. F., et al. (2002). Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1. Oncogene 21 4212–4219. 10.1038/sj.onc.1205610 - DOI - PubMed

[6] Albertoni M., Shaw P. H., Nozaki M., Godard S., Tenan M., Hamou M. F., et al. (2002). Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1. Oncogene 21 4212–4219. 10.1038/sj.onc.1205610 - DOI - PubMed

[7] Artz A., Butz S., Vestweber D. (2016). GDF-15 inhibits integrin activation and mouse neutrophil recruitment through the ALK-5/TGF-betaRII heterodimer. Blood 128 529–541. 10.1182/blood-2016-01-696617 - DOI - PubMed

[8] Artz A., Butz S., Vestweber D. (2016). GDF-15 inhibits integrin activation and mouse neutrophil recruitment through the ALK-5/TGF-betaRII heterodimer. Blood 128 529–541. 10.1182/blood-2016-01-696617 - DOI - PubMed

[9] Baek S. J., Kim K. S., Nixon J. B., Wilson L. C., Eling T. E. (2001). Cyclooxygenase inhibitors regulate the expression of a TGF-beta superfamily member that has proapoptotic and antitumorigenic activities. Mol. Pharmacol. 59 901–908. 10.1124/mol.59.4.901 - DOI - PubMed

[10] Baek S. J., Kim K. S., Nixon J. B., Wilson L. C., Eling T. E. (2001). Cyclooxygenase inhibitors regulate the expression of a TGF-beta superfamily member that has proapoptotic and antitumorigenic activities. Mol. Pharmacol. 59 901–908. 10.1124/mol.59.4.901 - DOI - PubMed

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GDF15 and Growth Control

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