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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.

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