Autophagy: A new therapeutic target for liver fibrosis

Mao, Yuqing; Fan, Xiaoming

doi:10.4254/wjh.v7.i16.1982

Cited by 42 publications

(33 citation statements)

References 32 publications

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“…Along with HSCs activation, autophagy flux is up‐regulated. Autophagy may supply energy for activation of HSCs by delivering triglyceride and other components in lipid drops from autophagosomes to lysosomes for degradation 19, 20. Hernández‐Gea et al .…”

Section: Discussionmentioning

confidence: 99%

“…Along with HSCs activation, autophagy flux is up-regulated. Autophagy may supply energy for activation of HSCs by delivering triglyceride and other components in lipid drops from autophagosomes to lysosomes for degradation [19,20]. Hern andez-Gea et al found that inhibition of autophagic function in primary mouse HSCs and mice following reduced fibrogenesis and matrix accumulation, which suggested autophagy promoted HSCs activation [21].…”

Section: Discussionmentioning

confidence: 99%

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Naringin in Ganshuang Granule suppresses activation of hepatic stellate cells for anti‐fibrosis effect by inhibition of mammalian target of rapamycin

Shi

Ren

Chen

et al. 2016

J Cellular Molecular Medi

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A previous study has demonstrated that Ganshuang granule (GSG) plays an anti‐fibrotic role partially by deactivation of hepatic stellate cells (HSCs). In HSCs activation, mammalian target of rapamycin (mTOR)‐autophagy plays an important role. We attempted to investigate the role of mTOR‐autophagy in anti‐fibrotic effect of GSG. The cirrhotic mouse model was prepared to demonstrate the anti‐fibrosis effect of GSG. High performance liquid chromatography (HPLC) analyses were used to identify the active component of GSG. The primary mouse HSCs were isolated and naringin was added into activated HSCs to observe its anti‐fibrotic effect. 3‐methyladenine (3‐MA) and Insulin‐like growth factor‐1 (IGF‐1) was added, respectively, into fully activated HSCs to explore the role of autophagy and mTOR. GSG played an anti‐fibrotic role through deactivation of HSCs in cirrhotic mouse model. The concentration of naringin was highest in GSG by HPLC analyses and naringin markedly suppressed HSCs activation in vitro, which suggested that naringin was the main active component of GSG. The deactivation of HSCs caused by naringin was not because of the autophagic activation but mTOR inhibition, which was supported by the following evidence: first, naringin induced autophagic activation, but when autophagy was blocked by 3‐MA, deactivation of HSCs was not attenuated or reversed. Second, naringin inhibited mTOR pathway, meanwhile when mTOR was activated by IGF‐1, deactivation of HSCs was reversed. In conclusion, we have demonstrated naringin in GSG suppressed activation of HSCs for anti‐fibrosis effect by inhibition of mTOR, indicating a potential therapeutic application for liver cirrhosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Naringin in Ganshuang Granule suppresses activation of hepatic stellate cells for anti‐fibrosis effect by inhibition of mammalian target of rapamycin

Shi

Ren

Chen

et al. 2016

J Cellular Molecular Medi

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“…TGF-beta (transforming growth factor-beta) signaling systems acting as major growth regulatory pathways crosstalk with mTOR-autophagy genes and apoptosis genes to control cell growth and death1920. In response to the crude extract vs. GCV, six genes related to the TGF-beta were deregulated, including four upregulated genes ( bmpr1aa, bmpr1ba, smad3a , and Rhoab ) and two downregulated genes ( Rhoaa and Rhoac ).…”

Section: Resultsmentioning

confidence: 99%

Tissue Extract Fractions from Starfish Undergoing Regeneration Promote Wound Healing and Lower Jaw Blastema Regeneration of Zebrafish

Dai

Prithiviraj

Gan

et al. 2016

Sci Rep

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Natural bioactive materials provide an excellent pool of molecules for regenerative therapy. In the present study, we amputate portions of the arms of Archaster typicus starfish, extract and separate the active biomaterials, and compare the effects of each fraction on in vitro wound healing and in vivo lower jaw regeneration of zebrafish. Compared with crude extract, normal hexane fractions (NHFs) have a remarkable effect on cellular proliferation and collective migration, and exhibit fibroblast-like morphology, while methanol-water fractions (MWFs) increase cell size, cell-cell adhesion, and cell death. Relative to moderate mitochondrialand lysosomal aggregation in NHFs-cultured cells, MWFs-cultured cells contain more and bigger lysosomal accumulations and clump detachment. The in vivo zebrafish lower jaw regeneration model reveals that NHFs enhance blastema formation and vasculogenesis, while MWFs inhibit fibrogenesis and induce cellular transformation. Gene expression analyses indicate that NHFs and MWFs separately activate blastema-characteristic genes as well as those genes-related to autophagy, proteasome, and apoptosis either during cell scratch healing or ganciclovir-induced apoptosis. Our results suggest that bioactive compounds from NHFs and MWFs could induce blastema formation and remodeling, respectively, and prevent tissue overgrowth.

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“…In most of the chronic liver diseases and liver fibrosis, there is significant increase in inflammation and stress followed by vascular remodelling because of extra cellular matrix deposition [2]. Liver injury occurs because of several factors among them the prominent are hepatitis B or hepatitis C virus infections, stress, xenobiotics, alcohol consumption, non-alcoholic steatohepatitis (NASH) [3]. The liver enzymes are unable to degrade scar tissue and the response goes inappropriate and resulting in deposition of more collagen and degradation of elastin in the development of fibrosis [4].…”

Section: Mini Reviewmentioning

confidence: 99%