Researchers from the School of Life Sciences of Nanjing University confirmed in a new study that the self-regulated feedback loop of miR-21 / PDCD4 / AP-1 is the driving force for the formation of liver fibrosis. )on.

Professor Lei Dong and Junfeng Zhang of the School of Life Sciences of Nanjing University are the co-corresponding authors of this paper. The main research direction of the former is biological therapy and disease pathogenesis research centered on macrophage nucleic acid drug targeting. The latter's research direction is biochemistry and biomedical engineering, mainly engaged in the research of genetic drugs and their delivery methods.

Fibrosis of liver is a pathological change caused by chronic liver damage caused by various reasons. It is manifested by excessive abnormal deposition of extracellular interstitial components in the liver and affects the function of the liver. The necessary stage. The current research focuses on the interaction between molecules and molecules, molecules and cells, and cells and cells. Although there has been some progress in diagnosis and treatment, there is still a lack of certain effective drugs. Liver fibrosis and its final stage of cirrhosis are major public health problems worldwide.

In the development of liver fibrosis, the activation of hepatic stellate cells (HSCs) plays a key role. After the liver is subjected to harmful stimulation, the resting HSCs are activated and transdifferentiated into myofibroblast-like cells, and then secrete a large amount of inflammatory factors and pro-fibrotic factors, which leads to excessive accumulation of extracellular matrix. At the same time, these secreted cytokines can also stimulate the proliferation of HSCs and inhibit their apoptosis, which ultimately leads to an increase in the degree of liver fibrosis. Although great progress has been made in understanding the mechanism of fiber formation in recent years, the potential driving force for this continuous fiber formation activity is still not clear.

Recent studies have found that miR-21 is generally up-regulated during the formation of different tissue fibers, but its detailed role remains to be clarified. Under different disease conditions, the expression of miR-21 is regulated by different upstream effectors. Studies have confirmed that AP-1 protein plays a role in the development of liver fibrosis. AP-1 protein can drive miR-21 expression, and miR-21-mediated PDCD4 down-regulation is a necessary condition for maximizing AP-1 activity. It is speculated that miR-21, PDCD4 and AP-1 may form a feedback loop during the activation of HSCs and promote the process of liver fibrosis.

In this article, the researchers tested miR-21 expression in human liver cirrhosis samples and mouse fibrotic liver induced by thioacetamide (TAA) or carbon tetrachloride (CCL4) and found that activated HSCs The miR-21 increased significantly. They further found that miR-21 maintains itself at a high level that is permanently maintained by using the miR-21 / PDCD4 / AP-1 feedback loop.

Using miR-21 antagonists (antagomir) or AP-1 inhibitors to disrupt this feedback loop can significantly inhibit the fiber formation activity in HSCs. In contrast, the use of small interfering RNA (siRNA) against PDCD4 to enhance this feedback loop can promote HSCs fiber formation. Further analysis showed that the up-regulation of miR-21 promoted the potentially important TGF-β signaling pathway of HSC activation.

These results indicate that the miR-21 / PDCD4 / AP-1 self-regulating loop is a major driver of liver fibrosis. Targeting this abnormally activated feedback loop may represent a new therapeutic strategy that will drive the discovery of therapeutic drugs for liver fibrosis.

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