Evidence for a role of microRNA‐146a in the pathogenesis of systemic lupus erythematosus with atherosclerosis: Comment on the article by Li et al

Xu, Wang‐Dong; Zhang, Yujing; Ye, Dong-Qing

doi:10.1002/art.33356

Cited by 3 publications

(1 citation statement)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, miR-1 is found to be high in expression, whereas miR-21 is found to be expressed lower in the pathogenesis of myocardial hypertrophy (26). miR146a has been found to play a critical role in pathological changes of atherosclerosis (28). miRNAs have also been found to be associated with the pathogenesis of diabetes (29).…”

Section: Discussionmentioning

confidence: 99%

Diabetes and hyperlipidemia induce dysfunction of VSMCs: contribution of the metabolic inflammation/miRNA pathway

Yang

Zhu

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Vascular endothelial cell injury is considered to be the major factor inducing vascular complications in metabolic diseases and plays an important role in other organ damage. With diabetic and hyperlipidemic rats and cultured VSMCs, the present study was aimed at investigating whether the early damage of VSMCs during metabolic diseases plays a critical role in vascular dysfunction and the underlying mechanisms and would be a promising treatment target. With diabetic and hyperlipidemic rats and cultured VSMCs, the changes and relationships of vascular relaxation and contractile function to the vital organ damage and the underlying mechanisms were investigated; meanwhile, the protective and preventive effects of lowering blood lipid and glucose and inhibition of diabetes and hyperlipidemia-induced vascular hyperreactivity were observed. Diabetic and hyperlipidemic rats presented hyperreactivity in vascular contractile response in the early stages. Hyperglycemia and hyperlipidemia directly affected the contractile function of VSMCs. Early application of fasudil, a specific antagonist of Rho kinase, significantly alleviated diabetes and hyperlipidemia-induced organ damage by inhibiting vascular hyperreactivity. Diabetes and hyperlipidemia-induced inflammatory response could upregulate the expression of connexins and Rho kinase by selective downregulation of the expression of miR-10a, miR-139b, miR-206, and miR-222. These findings suggest that hyperglucose and lipid may directly impair VSMCs and induce vascular hyperreactivity in the early stages. Metabolic inflammation-induced changes in the miRNA-connexin/Rho kinase regulatory pathway are the main mechanism for vascular hyperreactivity and organ damage. Measures inhibiting vascular hyperreactivity are promising for the prevention of organ damage induced by metabolic diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Diabetes and hyperlipidemia induce dysfunction of VSMCs: contribution of the metabolic inflammation/miRNA pathway

Yang

Zhu

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

show abstract

MicroRNA-126-5p inhibits apoptosis of endothelial cell in vascular arterial walls via NF‑κB/PI3K/AKT/mTOR signaling pathway in atherosclerosis

et al. 2022

View full text Add to dashboard Cite

Involvement of TLR2-MyD88 in abnormal expression of miR-146a in peripheral blood monocytes of patients with chronic hepatitis C

Zhang

Wang

Tong

et al. 2015

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

View full text Add to dashboard Cite

miR-146a is an immunoregulatory microRNA closely associated with viral infection. This study investigated the expression changes of miR-146a in peripheral blood monocytes of HCV-infected patients and the mechanism by which the THP-1 cells were stimulated with HCV core protein in vitro. It was found that in the peripheral blood monocytes of HCV-infected patients, miR-146a expression was upregulated. After treated by interferon/ribavirin, miR-146a expression was decreased when HCV RNA became undetectable. HCV core could directly stimulate THP-1 cells to produce miR-146a. Silencing TLR2 and MyD88 could significantly inhibit the expression of miR-146a. It was concluded that the expression of miR-146a in peripheral blood monocytes of HCV-infected patients was abnormally increased. The TLR2-MyD88 signaling pathway may take part in the overexpression of miR-146a in monocytes stimulated with HCV core protein.

show abstract

Evidence for a role of microRNA‐146a in the pathogenesis of systemic lupus erythematosus with atherosclerosis: Comment on the article by Li et al

Cited by 3 publications

References 11 publications

Diabetes and hyperlipidemia induce dysfunction of VSMCs: contribution of the metabolic inflammation/miRNA pathway

Diabetes and hyperlipidemia induce dysfunction of VSMCs: contribution of the metabolic inflammation/miRNA pathway

MicroRNA-126-5p inhibits apoptosis of endothelial cell in vascular arterial walls via NF‑κB/PI3K/AKT/mTOR signaling pathway in atherosclerosis

Involvement of TLR2-MyD88 in abnormal expression of miR-146a in peripheral blood monocytes of patients with chronic hepatitis C

Contact Info

Product

Resources

About