Evidence map›Paper›PMID 24492652›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2014

All-trans-retinoic acid improves cholestasis in α-naphthylisothiocyanate-treated rats and Mdr2-/- mice.

Shi-Ying Cai, Albert Mennone, Carol J Soroka, James L Boyer

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. The role of the retinoid receptor, RAR/RXR heterodimer, in liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Cenicriviroc, a cytokine receptor antagonist, potentiates all-trans retinoic acid in reducing liver injury in cholestatic rodents.Liver international : official journal of the International Association for the Study of the Liver · 2018
    Article
  11. Article
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Shi-Ying CaiDepartment of Internal Medicine and Yale Liver Center, Yale University School of Medicine, New Haven, Connecticut.
Albert Mennone
Carol J Soroka
James L Boyer
Yale University · US

Funding

Yale Liver CenterP30DK034989 · NIDDK · YALE UNIVERSITY · PI YASUKO IWAKIRI · 1986 to 2026
$31.1M
MECHANISMS OF BILE SECRETION &CHOLESTASISR37DK025636 · NIDDK · YALE UNIVERSITY · PI BOYER, JAMES LORENZEN · 1990 to 2017
$9.7M
NIDDK NIH HHS P30 DK034989NIDDK NIH HHS P30-DK34989NIDDK NIH HHS R37 DK025636NIDDK NIH HHS R37-DK25636
6 · The paper itself

Abstract

Chronic cholestasis results in liver injury and eventually liver failure. Although ursodeoxycholic acid (UDCA) showed limited benefits in primary biliary cirrhosis, there is an urgent need to develop alternative therapy for chronic cholestatic disorders. Previous studies from our laboratory demonstrated that all-trans-retinoic acid (atRA) is a potent suppressor of CYP7A1, the rate-limiting enzyme in bile acid synthesis. atRA also repressed the expression of tumor growth factor-β and collagen 1A1 in activated primary human stellate cells and LX2 cells. When administered together with UDCA to bile duct-ligated rats, this combined therapy significantly reduced the bile acid pool size and improved liver conditions. To further examine whether atRA alone or in combination with UDCA has greater beneficial effects than UDCA treatment alone, we assessed this treatment in two additional chronic cholestatic rodent models: α-naphthylisothiocyanate (ANIT)-treated rats and the Mdr2(-/-) (Abcb4(-/-)) knockout mouse. atRA alone significantly reduced bile duct proliferation, inflammation, and hydroxyproline levels in ANIT-treated rats, whereas the combination of atRA and UDCA significantly reduced plasma bile salt level compared with UDCA treatment. atRA alone or in combination with UDCA significantly reduced plasma levels of alkaline phosphatase and bile salts in 12-week-old Mdr2(-/-) mice. Reduced bile duct proliferation and inflammation were also observed in the livers of these mice. Together, atRA alone or in combination with UDCA significantly reduced the severity of liver injury in these two animal models, further supporting the combination treatment of atRA and UDCA as a potential new therapy for patients with chronic cholestatic liver disease who have not responded fully to UDCA.

Indexed as

1-NaphthylisothiocyanateAnimalsATP-Binding Cassette Sub-Family B Member 4ATP Binding Cassette Transporter, Subfamily BBile Acids and SaltsCell ProliferationCholagogues and CholereticsCholestasisChronic DiseaseDisease Models, AnimalDrug Therapy, CombinationLiverMaleMiceMice, KnockoutRats1-NaphthylisothiocyanateATP-Binding Cassette Sub-Family B Member 4ATP Binding Cassette Transporter, Subfamily BBile Acids and SaltsCholagogues and CholereticsTretinoinUrsodeoxycholic Acid

Identifiers

PMID24492652
PMCPMC3965885
OpenAlexW2157121141

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.