UCHL1 aggravates skin fibrosis through an IGF‐1‐induced Akt/mTOR/HIF‐1α pathway in keloid

Abstract

Keloids are fibroproliferative dermatoses characterized by the excessive production of extracellular matrix (ECM). The eruptions grow beyond the margin of the original wound and invade the surrounding tissues. The treatment is a great challenge for both clinicians and patients regarding the high frequency of recurrence and resistance. Researches have been amounted recently; however, the pathogenesis still remains poorly understood. 1,2 Fibroblasts are the crucial players in keloids and are featured by great heterogenicity with respect to numerous markers and signaling pathways. The heterogenicity attributes to race, age, location, disease duration, and stage, sampling sites such as margin, center, superficial or deep sites, test methods, and so on. 2 Despite the divergency, alpha-smooth muscle actin (α-SMA) and collagen I, the major extracellular matrix (ECM) components, are the fibrotic markers most frequently used in keloid studies. 3,4 Positive α-SMA fibroblasts are also known as

Endogenous stimuli-responsive separating microneedles to inhibit hypertrophic scar through remodeling the pathological microenvironment

“…Activation of the IGF1R by binding of IGF-1 and IGF-2 plays important roles in induction of proliferation, inhibition of cell apoptosis and induction of differentiation 52 . In addition, IGF1R is highly expressed in dermal fibroblasts of HS and keloid 53 , and IGF-1-induced AKT/mTOR/HIF-1α signaling pathway is involved in the pathogenesis of keloid 54 . Therefore, down-regulation of BAD and IGF1R pathways could promote fibroblast apoptosis, inhibit collagen synthesis and reverse skin fibrosis.…”

Effect of RNA interference with HIF-1α on the growth of pulmonary artery endothelial cells in broiler chickens

“…Studies have shown that collagen deposition thickens the triple-layer structure of pulmonary arteries and induces pulmonary hypertension ( Volkova et al, 2023 ). Inhibition of the HIF-1α signaling pathway reduces UCHL1-induced collagen expression in fibroblasts ( Guo et al, 2023 ). This further confirms that HIF-1α has the potential to regulate collagen expression to modulate the growth of PAECs and influence the development of ascites syndrome in broilers.…”