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MicroRNA Function in the Profibrogenic Interplay upon Chronic Liver Disease
被引:15
|作者:
Huang, Jia
[1
]
Yu, Xiaojie
[1
]
Fries, Jochen W. U.
[1
]
Zhang, Li'ang
[1
,2
,3
]
Odenthal, Margarete
[1
,2
]
机构:
[1] Univ Hosp Cologne, Inst Pathol, D-50924 Cologne, Germany
[2] Univ Cologne, Ctr Mol Med Cologne, D-50924 Cologne, Germany
[3] Univ Hosp Cologne, Clin Internal Med 1, D-50924 Cologne, Germany
关键词:
liver fibrosis;
myofibroblastic transition;
TGF-beta;
miRNA;
HEPATIC STELLATE CELLS;
NONALCOHOLIC STEATOHEPATITIS;
CANCER-DIAGNOSIS;
GROWTH-FACTOR;
EXPRESSION;
MIR-29;
ACTIVATION;
MECHANISMS;
INFECTION;
FIBROSIS;
D O I:
10.3390/ijms15069360
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
In chronic liver disease leading to fibrosis, hepatic stellate cells (HSC) differentiate into myofibroblasts. Myofibroblastic HSC have taken center stage during liver fibrogenesis, due to their remarkable synthesis of extracellular matrix proteins, their secretion of profibrogenic mediators and their contribution to hypertension, due to elevated contractility. MicroRNAs (miRNAs) are small, noncoding RNA molecules of 19-24 nucleotides in length. By either RNA interference or inhibition of translational initiation and elongation, each miRNA is able to inhibit the gene expression of a wide panel of targeted transcripts. Recently, it was shown that altered miRNA patterns after chronic liver disease highly affect the progression of fibrosis by their potential to target the expression of extracellular matrix proteins and the synthesis of mediators of profibrogenic pathways. Here, we underline the role of miRNAs in the interplay of the profibrogenic cell communication pathways upon myofibroblastic differentiation of hepatic stellate cells in the chronically injured liver.
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页码:9360 / 9371
页数:12
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