1. Academic Validation
  2. GDF15, an update of the physiological and pathological roles it plays: a review

GDF15, an update of the physiological and pathological roles it plays: a review

  • Pflugers Arch. 2020 Nov;472(11):1535-1546. doi: 10.1007/s00424-020-02459-1.
Artin Assadi 1 2 Azadeh Zahabi 3 Robert A Hart 4
Affiliations

Affiliations

  • 1 Department of Pilot Biotechnology, Pasteur Institute, Tehran, Iran.
  • 2 Department of Radiopharmacy, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
  • 3 Department of Oncology, Hematology, Immunology, Rheumatology, and Pulmonology, University Hospital Tuebingen, Hoppe-Seyler-Straße 3, Tübingen, 72076, Germany.
  • 4 School of Science and Technology, University of New England, McClymont Building, Armidale, NSW, 2351, Australia. rhart7@une.edu.au.
Abstract

Growth Differentiation Factor 15 (GDF15) is a peptide hormone, and a divergent member of the transforming growth factor beta (TGFβ) superfamily. In normal physiology, GDF15 is expressed in multiple tissues at a low concentration. GDF15 is overexpressed during and following many pathological conditions such as tissue injury and inflammation in order to play a protective role. However, GDF15 appears to promote tumour growth in the later stages of malignant Cancer. The recently identified endogenous receptor for GDF15, GDNF family receptor a-like (GFRAL), has allowed elucidation of a physiological pathway in which GDF15 regulates energy homeostasis and body weight, primarily via appetite suppression. The anorectic effect of GDF15 provides some therapeutic potential in management of cancer-related anorexia/cachexia and obesity. Despite the identification of GFRAL as a GDF15 receptor, there appears to be other signalling mechanisms utilized by GDF15 that further increase the possibility of development of therapeutic treatments, should these pathways be fully characterized. In this review, GDF15 function in both physiological and pathological conditions in various tissues will be discussed.

Keywords

Cancer; Energy homeostasis; GDF15; GFRAL; TGFβ.

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