Abstract
A keloid is a benign fibroproliferative skin tumor that results from abnormal wound healing after injury and tends to grow beyond the boundary of the original wound; the mechanism of keloid formation is still unclear. MicroRNA-21 (MiR-21) is a representative microRNA that plays a key role in a variety of fibrotic diseases via the transforming growth factor-β/Smad signaling pathway. The aim of our study was to explore the mechanism of keloid formation. First, we found that the expression of miR-21 in keloids and keloid fibroblasts was significantly upregulated by microRNA microarray and real-time polymerase chain reaction. Additionally, at the protein level, our study confirmed that the overexpression of miR-21 could promote the process of keloid fibrosis to some extent and also indicated that a low expression of miR-21 could inhibit the process of keloid fibrosis. Finally, the results proved that miR-21 could participate in the keloid fibrosis process through negative regulation of its downstream target gene Smad7 via the transforming growth factor-β/Smad signaling pathway, which provides a guiding framework for further studies and new theoretical support for keloid clinical treatment.
Interleukin17A Promotes Postoperative Cognitive Dysfunction by Triggering β-Amyloid Accumulation via the Transforming Growth Factor-β (TGFβ)/Smad Signaling Pathway
