Roseotoxin B alleviates cholestatic liver fibrosis through inhibiting PDGF-B/PDGFR-β pathway in hepatic stellate cells

  title={Roseotoxin B alleviates cholestatic liver fibrosis through inhibiting PDGF-B/PDGFR-$\beta$ pathway in hepatic stellate cells},
  author={Xingqi Wang and Yu-zhi Gao and Yu Li and Yuqing Huang and Yawen Zhu and Wei Lv and R Wang and Lingshan Gou and Chao Cheng and Zhaojun Feng and Jun Xie and Jun Tian and Ruiqin Yao},
  journal={Cell Death \& Disease},
Identifying effective anti-fibrotic therapies is a major clinical need that remains unmet. In the present study, roseotoxin B was shown to possess an improving effect on cholestatic liver fibrosis in bile duct–ligated mice, as proved by histochemical and immunohistochemical staining, hepatic biochemical parameters, and TUNEL apoptotic cell detection in tissue sections. Using cellular thermal shift assay, computational molecular docking, microscale thermophoresis technology, and surface plasmon… 

Cynarin inhibits PDGF-BB-induced proliferation and activation in hepatic stellate cells through PPARγ

Abstract Cynarin, a caffeoylquinic acid compound that was mainly extracted from Cynara scolymus L., displays various activities such as antioxidant, antibacterial, choleretic, and hepatoprotective

Therapy that Targets Growth Factor Receptors: Novel Approach for Liver Cirrhosis Treatment

This chapter represents the evidences of the efficacy of growth factor receptors signaling downregulation for the suppression of liver fibrosis and cirrhosis and their individual manifestations.

miR-488-5p mitigates hepatic stellate cell activation and hepatic fibrosis via suppressing TET3 expression

It is highlighted that miR-488-5p restrains the activation of HSCs and hepatic fibrosis via targeting TET3 which is involved in the TGF-β/Smad2/3 signaling pathway.

Progress in research on the roles of TGR5 receptor in liver diseases

The discovery of the regulatory relationship between the TGR5 receptor and miRNA-26a provides a new direction for further studies of the molecular mechanism underlying the effects of TGR7, and could have therapeutic implications for various liver diseases.

Pathogenesis of Liver Fibrosis and Its TCM Therapeutic Perspectives

The factors influencing liver fibrosis are described, focusing on the effects of cells, intestinal flora, iron death, signaling pathways, autophagy and angiogenesis on liver Fibrosis, and the therapeutic effects of herbal medicine on Liver fibrosis.

Identification of Liver Fibrosis-Related MicroRNAs in Human Primary Hepatic Stellate Cells Using High-Throughput Sequencing

The miRNAs identified may provide a basis and reference for the selection of diagnostic and therapeutic targets for hepatic fibrosis and the targeted genes were involved in collagen metabolism, extracellular matrix structural constituent, cytoskeletal protein binding, and cell adhesion.

Function of TREM1 and TREM2 in Liver-Related Diseases

The function of TREM1 and TREM2 in different liver diseases based on inflammation is reviewed, providing a more comprehensive perspective for the treatment of liver-related diseases.

The oncogenic potential of NANOG: An important cancer induction mediator

It is intended to demonstrate that targeting NANOG can dimmish the CSCs, sensitize the tumor to chemotherapy, and eradicate the cancer cells.



Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.

The role of a classical modulator of hepatocellular apoptosis in early, cholestatic liver injury is explored and these include activation of NF-κB and MAPK signaling, production of inflammatory cytokines, and recruitment of neutrophils in response to Cholestasis.

Liver fibrosis and hepatic stellate cells: Etiology, pathological hallmarks and therapeutic targets

The role of HSCs in liver fibrosis is outlined and novel strategies to suppress HSC activity are details, thereby providing new insights into potential treatments for liver Fibrosis.

Hepatic stellate cells as key target in liver fibrosis.

Mechanisms of hepatic stellate cell activation

These findings reinforce the remarkable complexity and plasticity of HSC activation, and underscore the value of clarifying its regulation in hopes of advancing the development of novel diagnostics and therapies for liver disease.

Hepatocyte TNF Receptor–Associated Factor 6 Aggravates Hepatic Inflammation and Fibrosis by Promoting Lysine 6–Linked Polyubiquitination of Apoptosis Signal‐Regulating Kinase 1

It is demonstrated that tumor necrosis factor receptor–associated factor 6 (TRAF6) promotes lysine 6 (Lys6)‐linked polyubiquitination and subsequent activation of ASK1 to trigger the release of robust proinflammatory and profibrotic factors in hepatocytes, which, in turn, drive HSC activation and hepatic fibrosis.

Regulation of PDGF and its receptors in fibrotic diseases.

  • J. Bonner
  • Medicine, Biology
    Cytokine & growth factor reviews
  • 2004

Anti-Apoptotic Effects of Recombinant Human Hepatocyte Growth Factor on Hepatocytes Were Associated with Intrahepatic Hemorrhage Suppression Indicated by the Preservation of Prothrombin Time

Results showed that the anti-apoptotic effect of rh-HGF on hepatocytes coincided strikingly with the suppression of intrahepatic hemorrhage, and prothrombin time was considered to be the best parameter that correlated with the intrahePatic hemorrhages associated with hepatocellular damage.