lncRNA GAS5 restrains CCl
Animals
Carrier Proteins
/ metabolism
Drug Discovery
Hepatic Stellate Cells
/ drug effects
Liver Cirrhosis
/ metabolism
MicroRNAs
/ genetics
PTEN Phosphohydrolase
/ metabolism
Proto-Oncogene Proteins c-akt
/ metabolism
RNA, Long Noncoding
/ genetics
RNA, Small Nucleolar
/ metabolism
Rats
Signal Transduction
/ drug effects
TOR Serine-Threonine Kinases
/ metabolism
Transforming Growth Factor beta
/ pharmacology
HSC
PTEN/PI3K/Akt signal pathway
hepatic fibrosis
lncRNA GAS5
miR-23a
Journal
American journal of physiology. Gastrointestinal and liver physiology
ISSN: 1522-1547
Titre abrégé: Am J Physiol Gastrointest Liver Physiol
Pays: United States
ID NLM: 100901227
Informations de publication
Date de publication:
01 04 2019
01 04 2019
Historique:
pubmed:
9
2
2019
medline:
25
12
2019
entrez:
9
2
2019
Statut:
ppublish
Résumé
Hepatic fibrosis is chronic liver damage with many causes that has a relatively high death rate. The current study showed that long noncoding RNA (lncRNA) growth arrest-specific transcript 5 (GAS5), microRNA-23a (miR-23a), and phosphatase and tensin homolog (PTEN) play important roles in the pathological process of hepatic fibrosis but have a relatively unclear regulatory mechanism. This study aimed to investigate the roles of lncRNA GAS5, miR-23a, and PTEN in the pathological process of hepatic fibrosis and hepatic stellate cell (HSC) activation. We used carbon tetrachloride (CCl
Identifiants
pubmed: 30735452
doi: 10.1152/ajpgi.00249.2018
doi:
Substances chimiques
Carrier Proteins
0
MIRN23 microRNA, rat
0
MicroRNAs
0
PI3KAP protein, rat
0
RNA, Long Noncoding
0
RNA, Small Nucleolar
0
Transforming Growth Factor beta
0
growth arrest specific transcript 5
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
PTEN Phosphohydrolase
EC 3.1.3.67
Pten protein, rat
EC 3.1.3.67
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM