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Thymosin-B4: a key modifier of renal disease

Vasilopoulou, Elisavet, Riley, Paul R, Long, David A (2018) Thymosin-B4: a key modifier of renal disease. Expert Opinion on Biological Therapy, . ISSN 1471-2598. (doi:10.1080/14712598.2018.1473371)

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Introduction: There is an urgent need for new treatments for chronic kidney disease (CKD). Thymosin-B4 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-B4 could be a novel therapeutic direction for CKD. Areas covered: Here, we review the current evidence on the actions of thymosin-B4 in the kidney in health and disease. Using transgenic mice, two recent studies have demonstrated that endogenous thymosin-B4 is dispensable for healthy kidneys. In contrast, lack of endogenous thymosin-B4 exacerbates mouse models of glomerular disease and angiotensin-II-induced renal injury. Administration of exogenous thymosin-B4, 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-B4 in the kidney and have shown promising results for the therapeutic potential of exogenous thymosin-B4 in CKD. Further studies should explore the mechanisms by which thymosin-B4 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.

Item Type: Article
DOI/Identification number: 10.1080/14712598.2018.1473371
Uncontrolled keywords: Ac-SDKP, cytoskeleton, fibrosis, glomerulus, inflammation, kidney disease, podocyte, thymosin-B4
Subjects: Q Science
Q Science > QP Physiology (Living systems)
Divisions: Faculties > Sciences > Medway School of Pharmacy
Depositing User: E. Vasilopoulou
Date Deposited: 08 Jun 2018 14:30 UTC
Last Modified: 29 May 2019 20:36 UTC
Resource URI: (The current URI for this page, for reference purposes)
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