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Thymosin-β4: A key modifier of renal disease

Vasilopoulou, E; Riley, PR; Long, DA; (2018) Thymosin-β4: A key modifier of renal disease. Expert Opinion on Biological Therapy , 18 (S1) pp. 185-192. 10.1080/14712598.2018.1473371. Green open access

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Abstract

INTRODUCTION: There is an urgent need for new treatments for chronic kidney disease (CKD). Thymosin-β4 is a peptide that reduces inflammation and fibrosis and has the potential to restore endothelial and epithelial cell injury, biological processes involved in the pathophysiology of CKD. Therefore, thymosin-β4 could be a novel therapeutic direction for CKD. Areas covered: Here, we review the current evidence on the actions of thymosin-β4 in the kidney in health and disease. Using transgenic mice, two recent studies have demonstrated that endogenous thymosin-β4 is dispensable for healthy kidneys. In contrast, lack of endogenous thymosin-β4 exacerbates mouse models of glomerular disease and angiotensin-II-induced renal injury. Administration of exogenous thymosin-β4, or its metabolite, Ac-SDKP, has shown therapeutic benefits in a range of experimental models of kidney disease. Expert opinion: The studies conducted so far reveal a protective role for thymosin-β4 in the kidney and have shown promising results for the therapeutic potential of exogenous thymosin-β4 in CKD. Further studies should explore the mechanisms by which thymosin-β4 modulates kidney function in different types of CKD. Ac-SDKP treatment has beneficial effects in many experimental models of kidney disease, thus supporting its potential use as a new treatment strategy.

Type: Article
Title: Thymosin-β4: A key modifier of renal disease
Location: England
Open access status: An open access version is available from UCL Discovery
DOI: 10.1080/14712598.2018.1473371
Publisher version: https://doi.org/10.1080/14712598.2018.1473371
Language: English
Additional information: This version is the author accepted manuscript. For information on re-use, please refer to the publisher’s terms and conditions.
Keywords: Ac-SDKP, cytoskeleton, fibrosis, glomerulus, inflammation, kidney disease, podocyte, thymosin-β4
UCL classification: UCL
UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Population Health Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Population Health Sciences > UCL GOS Institute of Child Health
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Population Health Sciences > UCL GOS Institute of Child Health > Developmental Biology and Cancer Dept
URI: https://discovery.ucl.ac.uk/id/eprint/10048228
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