INTRODUCTION
Keloid is a type of benign fibroproliferative skin disorder that results from excessive wound healing following skin trauma or inflammation and often extends beyond the original wound site, causing pain, itching, and significant cosmetic disfigurement.1,2 The pathogenesis of keloid is thought to involve abnormal fibroblast activation, excessive cell proliferation, and dysregulated extracellular matrix (ECM) deposition, while the exact contribution of myofibroblast-like cells is not fully clarified.3 Several important signaling pathways are involved in these processes, such as TGF-β/Smad, PI3K/AKT, mitogen-activated protein kinase (MAPK)/ERK, and JAK/STAT, which are implicated in keloid formation.4-6
Recently, various natural compounds have been investigated for their roles in the prevention and treatment of fibrotic diseases. Cardamonin (CARD), a natural agent extracted from Alpinia rafflesiana, is well known for its bioactivities in regulating inflammation, fibrosis, and other pathological processes.7 A previous study concluded that CARD can reduce myocardial fibrosis by suppressing collagen Ⅲ expression and NLR family pyrin domain containing 3 (NLRP3) inflammasome formation via AKT and ERK signaling pathways.8 Another study also revealed that CARD inhibited renal cyst development and interstitial fibrosis by downregulating TGF-β/Smad, mammalian target of rapamycin (mTOR), MAPK, and Wnt pathways.9 Additionally, CARD can delay the progression of pulmonary fibrosis by inhibiting the PI3K/AKT pathway.10 Although the various medicinal properties of CARD have been thoroughly researched in similar studies, the effect of CARD in the treatment of pathological skin scarring is still not fully explored.
Recently, various natural compounds have been investigated for their roles in the prevention and treatment of fibrotic diseases. Cardamonin (CARD), a natural agent extracted from Alpinia rafflesiana, is well known for its bioactivities in regulating inflammation, fibrosis, and other pathological processes.7 A previous study concluded that CARD can reduce myocardial fibrosis by suppressing collagen Ⅲ expression and NLR family pyrin domain containing 3 (NLRP3) inflammasome formation via AKT and ERK signaling pathways.8 Another study also revealed that CARD inhibited renal cyst development and interstitial fibrosis by downregulating TGF-β/Smad, mammalian target of rapamycin (mTOR), MAPK, and Wnt pathways.9 Additionally, CARD can delay the progression of pulmonary fibrosis by inhibiting the PI3K/AKT pathway.10 Although the various medicinal properties of CARD have been thoroughly researched in similar studies, the effect of CARD in the treatment of pathological skin scarring is still not fully explored.
