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Abstract
Therapies that modulate inflammation and fibrosis have the potential to reduce the morbidity and mortality associated with chronic kidney disease (CKD). A promising avenue may be manipulating thymosin-β4, a naturally occurring peptide, which is the major G-actin sequestering protein in mammalian cells and a regulator of inflammation and fibrosis. Thymosin-β4 is already being tested in clinical trials for heart disease and wound healing. This editorial outlines the evidence that thymosin-β4 may also have therapeutic benefit in CKD.
Declaration of interest
This paper is part of a supplemental issue, sponsored by SciClone. Support for this work was provided by a Kidney Research UK Senior Non-Clinical Fellowship (SF1/2008, to DAL), a Medical Research Council New Investigator Award (MR/J003638/1, to DAL) and the British Heart Foundation (CH/11/128798, to PRR). The authors have no other relevant affiliations or financial involvement with any organisation or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.