Angiotensin receptors in Dupuytren's tissue: Implications for the pharnnacological treatment of Dupuytren's disease

Abstract

The role of Angiotensin II as a pro-fibrotic mediator has been established in models of cardiac, hepatic and renal fibrosis. The administration of Angiotensin-Converting Enzyme (ACE) – inhibitors to these models results in a reduction in the myofibroblast population and collagen synthesis. In rodent excisionat wound-healing experiments, an ACE inhibitor reduced the rate of wound contraction, collagen deposition and angiogenesis. Using immunohistochemistry, the presence of Angiotensin I receptors was identified within tissue samples from patients with Dupuytren's disease. These were found to be co-localised with areas of myofibrobtast expression. This co-localisation has implications for the potential of pharmacological regulation of Dupuytren's disease. Further research is necessary to confirm whether the use of ACE-inhibitors can modulate this disease process, which until now has not been responsive to safe, effective pharmacological treatment.