Evidence map›Paper›PMID 29197066›Full record

ArticleBritish journal of pharmacology2018

Characterization of the properties of a selective, orally bioavailable autotaxin inhibitor in preclinical models of advanced stages of liver fibrosis.

Manuel Baader, Tom Bretschneider, Andre Broermann, Joerg F Rippmann, Birgit Stierstorfer, Christian A Kuttruff, Michael Mark

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. GPAT1 Deficiency in Mice Modulates NASH Progression in a Model-Dependent Manner.Cellular and molecular gastroenterology and hepatology · 2024
    Article
  3. Article
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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

7 authors at 1 institution in 1 country.

Manuel BaaderBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.ORCID 0000-0001-8772-712X
Tom BretschneiderBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Andre BroermannBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Joerg F RippmannBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Birgit StierstorferBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Christian A KuttruffBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Michael MarkBoehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.
Boehringer Ingelheim (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAutotaxin (ATX) is a secreted phospholipase which hydrolyses lysophosphatidylcholine to generate lysophosphatidic acid (LPA). The extracellular signalling molecule LPA exerts its biological actions through activation of six GPCRs expressed in various cell types including fibroblasts. Multiple preclinical studies using knockout animals, LPA receptor antagonists or ATX inhibitors have provided evidence for a potential role of the ATX/LPA axis in tissue fibrosis. Despite growing evidence for a correlation between ATX levels and the degree of fibrosis in chronic liver diseases, including viral hepatitis and hepatocellular carcinoma, the role of ATX in non-alcoholic steatohepatitis (NASH) remains unclear. EXPERIMENTAL APPROACH: The relevance of ATX in the pathogenesis of liver fibrosis was investigated by oral administration of Ex_31, a selective ATX inhibitor, in a 10 week model of carbon tetrachloride-induced liver injury and in a 14 week model of choline-deficient amino acid-defined diet-induced liver injury in rats. KEY

resultsOral administration of Ex_31, a selective ATX inhibitor, at 15 mg·kg CONCLUSIONS AND IMPLICATIONS: Our findings question the role of ATX in the pathogenesis of hepatic fibrosis and the potential of small molecule ATX inhibitors for the treatment of patients with NASH and advanced stages of liver fibrosis.

Indexed as

Administration, OralAnimalsBiological AvailabilityCaco-2 CellsCarbon TetrachlorideDrug Evaluation, PreclinicalHepatic Stellate CellsHumansLiver CirrhosisLysophospholipase DLysophospholipidsMalePhosphoric Diester HydrolasesRatsRats, Sprague-DawleyCarbon Tetrachloridelysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester Hydrolases

Identifiers

PMID29197066
PMCPMC5787030
OpenAlexW2772036759

What Socratic 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 Socratic graph.