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The renin-angiotensin system in cutaneous hypertrophic scar and keloid formation

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eMediNexus    08 August 2020

A new article published in Experimental Dermatology discussed that hypertrophic scar and keloid are two types of fibroproliferative disorders that result from excessive extracellular matrix production. Although the underlying mechanism is not entirely clear, it has been proposed that the activation of the renin-angiotensin system (RAS) is involved in their pathologenesis—as it influences fibrosis in various organs.

The authors elaborated that RAS components including angiotensin II (Ang II), angiotensin AT1 and AT2 receptors, and angiotensin-converting enzyme (ACE) are expressed in the skin and act independently from the plasma RAS. AT1 receptors—which are usually the dominating receptor subtype—promote fibrosis and scar formation, while AT2 receptors inhibit the aforementioned AT1 receptor-coupled effects. Elevated angiotensin II (Ang II) levels acting on the AT1 receptor contribute to skin scar formation through increased expression of inflammatory factors – such as, interleukin-6 (IL-6); angiogenic factors – such as, vascular endothelial growth factor (VEGF); and fibrinogenic factors – such as, transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF), while at the same time, suppressing the anti-fibrotic tissue inhibitors of matrix metalloproteinase (TIMPs).

This article reported that small clinical trials have provided evidence that inhibition of the ACE/Ang II/ AT1 receptor axis may be effective in the treatment of hypertrophic scars/keloids.

Source: Experimental Dermatology. 2020 Jul 17.doi: 10.1111/exd.14154.

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