Glucocorticoid promotes of lipid metabolism and mitophagy in human hypertrophic scar cells via microRNAs
Hypertrophic scar (HS) is a skin lesion due to abnormal wound healing after skin injury; histologically, HS is characterized by deposition of excessive amounts of the extracellular matrix and collagen produced by wound healing-induced proliferative fibroblasts. Clinically, HS management includes surgical resection of HS, topical glucocorticoid therapy or drug injections, pressure therapy, fractional carbon dioxide laser therapy, and cryotherapy. In terms of non-surgical therapy, glucocorticoids (like Triamcinolone acetonide, a synthetic corticosteroid medication used topically to treat various skin conditions) was able to effectively inhibit HS formation safely for decades. The effects of glucocorticoids may either be due to its anti-inflammatory, anti-allergenic and immunomodulatory effects or activate fatty acids metabolism by promotion of lipid accumulation in fibroblasts. However, it is no clear why and how glucocorticoids-upregulated fatty acid metabolisms benefit in HS treatment and prevention. It remains to be defined how altered microRNAs regulated-fatty acid metabolism involved in human hypertrophic scar cells.