Thymosin beta 4 regulation of actin in sepsis.
Recommended Citation
Belsky JB, Rivers EP, Filbin MR, Lee PJ, and Morris DC. Thymosin beta 4 regulation of actin in sepsis. Expert Opin Biol Ther 2018.
Document Type
Article
Publication Date
7-1-2018
Publication Title
Expert opinion on biological therapy
Abstract
INTRODUCTION: Sepsis is the dysregulated host response to an infection resulting in life-threatening organ damage. Thymosin Beta 4 is an actin binding protein that inhibits the polymerization of G-actin into F-actin and improves mortality when administered intravenously to septic rats. Thymosin Beta 4 decreases inflammatory mediators, lowers reactive oxygen species, up-regulates anti-oxidative enzymes, anti-inflammatory genes, and anti-apoptotic enzymes making it an interesting protein to study in sepsis.
AREAS COVERED: The authors summarize the current knowledge of actin and Thymosin Beta 4 as it relates to sepsis via a comprehensive literature search.
EXPERT OPINION: Sepsis results in measurable levels of F-actin in the circulation as well as a decreased concentration of Thymosin Beta 4. It is speculated that F-actinemia contributes to microcirculatory perturbations present in patients with sepsis by disturbing laminar flow. Given that Thymosin Beta 4 inhibits the polymerization of F-actin, it is possible that Thymosin Beta 4 decreases mortality in sepsis via the regulation of actin as well as its other anti-inflammatory properties and should be further pursued as a clinical trial in humans with sepsis.
Medical Subject Headings
Actins; Animals; Humans; Microcirculation; Oxidation-Reduction; Rats; Reactive Oxygen Species; Sepsis; Thymosin
PubMed ID
29508629
Volume
18
Issue
sup1
First Page
193
Last Page
197