Abstract | UNLABELLED: CONCLUSION: By demonstrating that a PPARalpha-independent fenofibrate-AMPK-SHP regulatory cascade can play a key role in PAI-1 gene down-regulation and reversal of fibrosis, our study suggests that various AMPK activators regulating SHP might provide a novel pharmacologic option in ameliorating hepatic metabolic syndromes.
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Authors | Dipanjan Chanda, Chul Ho Lee, Yong-Hoon Kim, Jung-Ran Noh, Don-Kyu Kim, Ji-Hoon Park, Jung Hwan Hwang, Mi-Ran Lee, Kyeong-Hoon Jeong, In-Kyu Lee, Gi Ryang Kweon, Minho Shong, Goo-Taeg Oh, John Y L Chiang, Hueng-Sik Choi |
Journal | Hepatology (Baltimore, Md.)
(Hepatology)
Vol. 50
Issue 3
Pg. 880-92
(Sep 2009)
ISSN: 1527-3350 [Electronic] United States |
PMID | 19593819
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cytokines
- PPAR alpha
- Plasminogen Activator Inhibitor 1
- Pyrimidines
- Receptors, Cytoplasmic and Nuclear
- Transcription Factors
- Transforming Growth Factor beta
- nuclear receptor subfamily 0, group B, member 2
- pirinixic acid
- AMP-Activated Protein Kinases
- Fenofibrate
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Topics |
- AMP-Activated Protein Kinases
(physiology)
- Animals
- Carcinoma, Hepatocellular
(metabolism)
- Cell Line, Tumor
- Cytokines
(antagonists & inhibitors)
- Fenofibrate
(pharmacology)
- Male
- Mice
- Mice, Inbred C57BL
- PPAR alpha
(agonists)
- Plasminogen Activator Inhibitor 1
(biosynthesis, metabolism)
- Pyrimidines
(pharmacology)
- Rats
- Receptors, Cytoplasmic and Nuclear
(physiology)
- Signal Transduction
- Transcription Factors
(antagonists & inhibitors)
- Transforming Growth Factor beta
(antagonists & inhibitors)
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