Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1832, Issue 7, Pages 905-910Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbadis.2012.09.009
Keywords
Fibrosis; Serotonin
Funding
- UK Medical Research Council
- Wellcome Trust
- European Council
- Newcastle University
- Medical Research Council [G0900535, G0700890, G0401643] Funding Source: researchfish
- MRC [G0401643, G0900535, G0700890] Funding Source: UKRI
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The molecule serotonin (5-hydroxytryptamine or 5-HT) is involved in numerous biological processes both inside and outside of the central nervous system. 5-HT signals through 5-HT receptors and it is the diversity of these receptors and their subtypes that give rise to the varied physiological responses. It is clear that platelet derived serotonin is critical for normal wound healing in multiple organs including, liver, lung heart and skin. 5-HT stimulates both vasoconstriction and vasodilation, influences inflammatory responses and promotes formation of a temporary scar which acts as a scaffold for normal tissue to be restored. However, in situations of chronic injury or damage 5-HT signaling can have deleterious effects and promote aberrant wound healing resulting in tissue fibrosis and impaired organ regeneration. This review highlights the diverse actions of serotonin signaling in the pathogenesis of fibrotic disease and explores how modulating the activity of specific 5-HT receptors, in particular the 5-HT2 subclass could have the potential to limit fibrosis and restore tissue regeneration. This article is part of a Special Issue entitled: Fibrosis: Translation of basic research to human disease. (C) 2012 Elsevier B.V. All rights reserved.
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