Liver sinusoidal endothelial cells as potential drivers of liver fibrosis (Review).

Liver fibrosis due to viral or metabolic chronic liver diseases is a major challenge of global health. It is a critical pre­stage condition of severe hepatopathy, characterized by excessive accumulation of extracellular matrix components and ongoing chronic inflammation. To date, early prevention of liver fibrosis remains challenging. As the most abundant non­parenchymal hepatic cell population, liver sinusoidal endothelial cells (LSECs) are stabilizers that maintain the intrahepatic environment. Notably, LSECs dysfunction appears to be implicated in the progression of liver fibrosis via numerous mechanisms. Following sustained liver injury, they lose their fenestrae (cytoplasmic pores) and change their crosstalk with other cellular interactions in the hepatic blood environment. LSEC­targeted therapy has shown promising effects on fibrosis resolution, opening up new opportunities for anti­fibrotic therapy. In light of this, the present study summarized changes in LSECs during liver fibrosis and their interactions with hepatic milieu, as well as possible therapeutic approaches that specially target LSECs.

Viral long non-coding RNA regulates virus life-cycle and pathogenicity.

Viral infection is still a serious global health problem that kills hundreds of thousands of people annually. Understanding the mechanism by which virus replicates, packages, and infects the host cells can provide new strategies to control viral infection. Long non-coding RNAs (lncRNAs) have been identified as critical regulators involved in viral infection process and antiviral response. A lot of host lncRNAs have been identified and shown to be involved in antiviral immune response during viral infection. However, our knowledge about lncRNAs expressed by viruses is still at its infancy. LncRNAs expressed by viruses are involved in the whole viral life cycle, including promoting genome replication, regulating gene expression, involvement in genome packaging, assembling new viruses and releasing virions to the host cells. Furthermore, they enhance the pathogenicity of viral infections by down-regulating the host cell's antiviral immune response and maintain the viral latency through a refined procedure of genome integration. This review focuses on the regulatory roles of viral lncRNA in the life-cycle and pathogenicity of viruses. It gives an insight into the viral lncRNAs that can be utilized as therapeutic targets against viral diseases, and future researches aimed to identify and explore new viral lncRNAs and the mechanisms of their involvement in viral infection is encouraged.