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

Abstract

Deep cutaneous injuries such as burn injuries, physical trauma, surgical incisions, vaccinations, skin piercings and even insect bites occasionally produce hypertrophic scars or keloids. It has been estimated that over 100 million people annually suffer from scar-related complications that significantly impair their quality of life. [1,2] These issues include cosmetic problems, functional disabilities such as contractures, and symptoms including pruritus and pain. [1] Although the clinical course, physical appearance and pathophysiological features

More than just bricks and mortar: Fibroblasts and ECM in skin health and disease

“…Hypertrophic scars and keloids are the two major types of fibrotic skin pathologies induced in response to wounding. Their mechanisms, similarities and differences have been the subject of intense research, as exemplified by recent papers in Experimental Dermatology 59–64 . This topic is also highlighted in several reviews in this issue.…”

Towards a renaissance of dermatoendocrinology: Selected current frontiers

“…The authors explain why the RAS invites novel interventions in dermatological therapy that still await systematic preclinical and clinical exploration. This is complemented by a paper by Hedayatyanfard et al, [63] which focuses on the role of the RAS in skin fibrosis, hypertrophic scars and keloid disease, and how the RAS may be therapeutically targeted in these conditions. This nicely complements earlier relevant work published in Experimental Dermatology, [22,[64][65][66] documenting the journal's persistent commitment to dermatoendocrinological research off-the-beaten track.…”

Therapeutic Strategies by Regulating Interleukin Family to Suppress Inflammation in Hypertrophic Scar and Keloid

“…By acting on AT1 receptor (Mulrow. 1999), angiotensin II promoted fibrosis, induced migration and proliferation of keratinocytes and fibroblasts, and increased collagen production through IL-6/TGF-β and AP-1/TGF-β pathways (Hedayatyanfard et al, 2020). The activation of AT2 receptor inhibited the above-mentioned process by blocking the expression of IL-6, TNF-α and TGF-β, and played an antiinflammatory role (Hedayatyanfard et al, 2020).…”