![]() The mechanisms underlying the regulation of the keloid microenvironment have not been fully explored. The keloid microenvironment includes keratinocytes, fibroblasts, vascular endothelial cells, immune cells, and stem cells with irregularly oriented collagen fibers (Fig. ![]() Increasing evidence has shown that keloids exhibit cellular bioenergetics, genetic and epigenetic changes and EMT processes that are similar to those in cancers to some extent. Various interactions between the components of the keloid microenvironment have been explored, which may explain the aggressive clinical behavior of keloids. Keloids are classified as a benign fibroproliferative dermal disease, though they exhibit some cancer-like behaviors, such as invasion of neighboring tissues and a high recurrence rate. IL-6 can also promote epithelial-mesenchymal transition (EMT) via the JAK/STAT pathway in keloid pathogenesis. Increased expression of the proinflammatory cytokines IL-6 and IL-8 and decreased expression of the anti-inflammatory cytokine IL-10 promote scarring, which is mediated by the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway. Keloids have high infiltration of profibrotic immune cells, such as M2 macrophages and Th2 cells, which promote fibroblast activation via the TGF-β1 signaling pathway. Multiple hypotheses for keloid formation have been suggested, such as dysregulation of inflammatory signaling pathways, the transforming growth factor β (TGF-β)/small mothers against decapentaplegic (Smad) signaling pathways, and the Yes-associated protein (YAP)/transcriptional coactivator with a PDZ-binding domain (TAZ) signaling pathway. Keloid formation is influenced by various factors, such as wound tension, genetic factors (age, race, family history), hormone levels, and lifestyle. To identify keloid-specific pathogenetic processes, we aimed to identify more specific therapeutic targets for keloids. As is observed in the clinic, keloids are often refractory to treatment thus, the treatment of keloids is a significant therapeutic challenge. ![]() Unfortunately, there is very low-certainty evidence to support the effectiveness of these laser therapies for treating keloids. Pulsed dye lasers include carbon dioxide (CO2) lasers, 585-nm pulsed-dye lasers, and neodymium-doped yttrium aluminum garnet (Nd:YAG) lasers. Local radiation therapies include electron beam radiotherapy and low- or high-dose-rate brachytherapy. In addition to corticosteroids, injectables also include 5-fluorouracil, botulinum toxin, verapamil, and avotermin. Surgical resection with postoperative radiation or adjuvant pharmacotherapies, radiation therapies, oral medications and laser-based therapies are also used to treat keloids. There are currently various treatment options for keloids, and silicone gel with intralesional corticosteroid injections is first recommended. Life quality of keloid patients is dramatically affected by physical symptoms, including pruritus and pain, as well as psychological barriers. Keloids are characterized by the excessive deposition of collagen during abnormal wound healing, which leads to a fibroproliferative inflammatory response with neovascularization at the leading edge. In this review, we summarized the nature of genetic and epigenetic regulation in keloid-derived fibroblasts, epithelial-to-mesenchymal transition of keratinocytes, immune cell infiltration into keloids, the differentiation of keloid-derived stem cells, endothelial-to-mesenchymal transition of vascular endothelial cells, extracellular matrix synthesis and remodeling, and uncontrolled angiogenesis in keloids with the aim of identifying new targets for therapeutic benefit. Recent advances in the study of keloids have led to novel insights into cellular communication among components of the keloid microenvironment as well as potential therapeutic targets for treating keloids. The keloid microenvironment is composed of keratinocytes, fibroblasts, myofibroblasts, vascular endothelial cells, immune cells, stem cells and collagen fibers. Keloids exhibit some cancer-like behaviors, with similar genetic and epigenetic modifications in the keloid microenvironment. Keloids are a fibroproliferative skin disorder that develops in people of all ages.
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