miR-146a contributes to atherosclerotic plaque stability by regulating the expression of TRAF6 and IRAK-1

Atherosclerotic three-layer nanomatrix vascular sheets for high-throughput therapeutic evaluation

“…Meanwhile, our VSA assays demonstrated that colchicine downregulated VEGF-A, suggesting that colchicine may inhibit angiogenesis and neovascularization in addition to its known effects of increasing plaque stability and regulating macrophage phenotype in treating atherosclerosis. For miR-146a, using our VSA assay, we obtained similar results as those found in the atherosclerotic mouse model, where miR-146a downregulated gene expression of IL-1β, IL-6, and TNF-α [ 81 ]. Significantly, the improved efficacy of microRNA transfection by using liposomes was also detected by our VSA assay, demonstrating its potential to evaluate drug delivery carrier-based formulations for atherosclerosis treatment.…”

Association between microRNA-146a rs2910164 polymorphism and coronary heart disease: An updated meta-analysis

“…[31] Meanwhile, the miR-146a could maintain the stability of atherosclerotic plaques by inhibiting the expression of interleukin-1 receptor-associated kinase 1 (IRAK-1) and tumor necrosis factor receptor-associated factor 6 (TRAF-6) in animal models. [32] Moreover, miR-146a was also meaningfully upgraded in patients' atherosclerotic plaques. [33] MiR-146a precursor with C allele sequence could downgrade the level of mature miR-146a by influencing the secondary structure compared with the G allele sequence.…”

“…[ 31 ] Meanwhile, the miR-146a could maintain the stability of atherosclerotic plaques by inhibiting the expression of interleukin-1 receptor-associated kinase 1 (IRAK-1) and tumor necrosis factor receptor-associated factor 6 (TRAF-6) in animal models. [ 32 ] Moreover, miR-146a was also meaningfully upgraded in patients’ atherosclerotic plaques. [ 33 ]…”

A comprehensive insight into the immunomodulatory role of MSCs‐derived exosomes (MSC‐Exos) through modulating pattern‐recognition receptors (PRRs)

“…This miRNA functions as a negative feedback regulator, aiding in the mitigation of undue inflammation. Notably, studies have revealed the presence of miR‐146a within MSC‐Exos, potentially substantiating their immunosuppressive properties 69,70 . Another MSC‐Exos‐derived microRNA is miR‐21, which has been documented as impacting TLR signaling.…”

“…Notably, studies have revealed the presence of miR-146a within MSC-Exos, potentially substantiating their immunosuppressive properties. 69,70 Another MSC-Exos-derived microRNA is miR-21, which has been documented as impacting TLR signaling. It can suppress TLR4 expression and the subsequent downstream signaling events, attenuating proinflammatory responses.…”