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Targeting Gut-Liver Axis for Treatment of Liver Fibrosis and Portal Hypertension
被引:4
|作者:
Kalo, Eric
[1
]
Read, Scott
[1
,2
,3
]
Ahlenstiel, Golo
[1
,2
,3
]
机构:
[1] Western Sydney Univ, Blacktown Clin Sch, Sch Med, Blacktown, NSW 2148, Australia
[2] Blacktown Hosp, Blacktown, NSW 2148, Australia
[3] Univ Sydney, Westmead Inst Med Res, Storr Liver Ctr, Westmead, NSW 2145, Australia
来源:
关键词:
liver fibrosis;
portal hypertension;
microbiota;
cirrhosis;
chronic liver disease;
gut-liver axis;
bacterial translocation;
hepatic macrophages;
PRRs;
TLRs;
INTERNATIONAL SCIENTIFIC ASSOCIATION;
AGONIST OBETICHOLIC ACID;
HEPATIC STELLATE CELLS;
RECEPTOR;
4;
ANTAGONIST;
TOLL-LIKE RECEPTOR-3;
BACTERIAL TRANSLOCATION;
FXR AGONIST;
INTESTINAL DECONTAMINATION;
PROBIOTIC VSLNUMBER-3;
KUPFFER CELLS;
D O I:
10.3390/livers1030014
中图分类号:
R57 [消化系及腹部疾病];
学科分类号:
摘要:
Antifibrotic therapies for the treatment of liver fibrosis represent an unconquered area of drug development. The significant involvement of the gut microbiota as a driving force in a multitude of liver disease, be it pathogenesis or fibrotic progression, suggest that targeting the gut-liver axis, relevant signaling pathways, and/or manipulation of the gut's commensal microbial composition and its metabolites may offer opportunities for biomarker discovery, novel therapies and personalized medicine development. Here, we review potential links between bacterial translocation and deficits of host-microbiome compartmentalization and liver fibrosis that occur in settings of advanced chronic liver disease. We discuss established and emerging therapeutic strategies, translated from our current knowledge of the gut-liver axis, targeted at restoring intestinal eubiosis, ameliorating hepatic fibrosis and rising portal hypertension that characterize and define the course of decompensated cirrhosis.
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页码:147 / 179
页数:33
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