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

@article{Wang2020RoseotoxinBA,
  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 W. Lv and Ruzeng Wang and Lingshan Gou and Chao Cheng and Zhaojun Feng and Jun Xie and Jun Tian and Ruiqin Yao},
  journal={Cell Death \& Disease},
  year={2020},
  volume={11}
}
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… 
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References

SHOWING 1-10 OF 42 REFERENCES
The PDGF system and its antagonists in liver fibrosis.
TLDR
This narrative review aims to gauge the recent progression of research into PDGF systems and liver fibrosis by identifying some multikinase inhibitors targeting PDGF signaling that are on the way into advanced preclinical studies and clinical trials.
Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.
TLDR
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
TLDR
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.
TLDR
Cell type- and target-specific pharmacological intervention to therapeutically induce the deactivation of hepatic stellate cells will enable more effective and less toxic precision antifibrotic therapies.
Mechanisms of hepatic stellate cell activation
TLDR
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.
The hepatocyte-specifically expressed lnc-HSER alleviates hepatic fibrosis by inhibiting hepatocyte apoptosis and epithelial-mesenchymal transition
TLDR
A hepatocyte-specific lnc-HSER is identified that regulates liver fibrosis, providing a proof that this molecule is a novel biomarker for damaged HCs and a potential target for anti-fibrotic therapy.
Pathophysiology of liver fibrosis and the methodological barriers to the development of anti-fibrogenic agents.
TLDR
Novel in-vitro models mimicking the interplay between pro-fibrogenic cell populations, immune cells and, importantly, the extracellular matrix need to be developed in order to identify an efficient anti-f fibrogenic compound.
Hepatocyte TNF Receptor–Associated Factor 6 Aggravates Hepatic Inflammation and Fibrosis by Promoting Lysine 6–Linked Polyubiquitination of Apoptosis Signal‐Regulating Kinase 1
Activation of apoptosis signal‐regulating kinase 1 (ASK1) is a key driving force of the progression of nonalcoholic steatohepatitis (NASH) and represents an attractive therapeutic target for NASH…
Fate-tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its etiology
TLDR
It is demonstrated that hepatic stellate cells give rise to 82-96% of myofibroblasts in models of toxic, cholestatic and fatty liver disease, and HSCs should be considered the primary cellular target for anti-fibrotic therapies across all types of liver disease.
Liver fibrosis: Pathophysiology, pathogenetic targets and clinical issues.
TLDR
This review will analyze the most relevant established and/or emerging pathophysiological issues underlying CLD progression with a focus on the role of critical hepatic cell populations, mechanisms and signaling pathways involved, as they represent potential therapeutic targets to finally analyze selected and relevant clinical issues.
...
1
2
3
4
5
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