Evidence map›Paper›PMID 27060337›Full record

ReviewJournal of thrombosis and haemostasis : JTH2016

Role of hemostatic factors in hepatic injury and disease: animal models de-liver.

A K Kopec, N Joshi, J P Luyendyk

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of thrombosis and haemostasis : JTH, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.8field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Antifungal Activity and Acute and Repeated-Dose Toxicity Study of Geranyl Cinnamate Ester in Mice.Evidence-based complementary and alternative medicine : eCAM · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

3 authors at 1 institution in 1 country.

A K KopecDepartment of Pathobiology & Diagnostic Investigation, Michigan State University, East Lansing, MI, USA.
N JoshiDepartment of Pharmacology & Toxicology, Michigan State University, East Lansing, MI, USA.
J P LuyendykDepartment of Pathobiology & Diagnostic Investigation, Michigan State University, East Lansing, MI, USA.
Michigan State University · US

Funding

Novel anti-fibrotic mechanisms in chemical-induced liver injuryR01ES017537 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUYENDYK, JAMES P · 2009 to 2019
$3.6M
Novel mechanisms stimulating liver repair after acetaminophen overdoseR01DK105099 · NIDDK · MICHIGAN STATE UNIVERSITY · PI LUYENDYK, JAMES P · 2015 to 2018
$1.4M
NIDDK NIH HHS R01 DK105099NIEHS NIH HHS R01 ES017537
6 · The paper itself

Abstract

Chronic liver damage is associated with unique changes in the hemostatic system. Patients with liver disease often show a precariously rebalanced hemostatic system, which is easily tipped towards bleeding or thrombotic complications by otherwise benign stimuli. In addition, some clinical studies have shown that hemostatic system components contribute to the progression of liver disease. There is a strong basic science foundation for clinical studies with this particular focus. Chronic and acute liver disease can be modeled in rodents and large animals with a variety of approaches, which span chronic exposure to toxic xenobiotics, diet-induced obesity, and surgical intervention. These experimental approaches have now provided strong evidence that, in addition to perturbations in hemostasis caused by liver disease, elements of the hemostatic system have powerful effects on the progression of experimental liver toxicity and disease. In this review, we cover the basis of the animal models that are most often utilized to assess the impact of the hemostatic system on liver disease, and highlight the role that coagulation proteases and their targets play in experimental liver toxicity and disease, emphasizing key similarities and differences between models. The need to characterize hemostatic changes in existing animal models and to develop novel animal models recapitulating the coagulopathy of chronic liver disease is highlighted. Finally, we emphasize the continued need to translate knowledge derived from highly applicable animal models to improve our understanding of the reciprocal interaction between liver disease and the hemostatic system in patients.

Indexed as

HemostasisAnimalsBile DuctsBlood CoagulationBlood Coagulation DisordersCarbon TetrachlorideChemical and Drug Induced Liver InjuryCholestasisChronic DiseaseDisease Models, AnimalHemorrhageHemostaticsHumansLiverLiver DiseasesMiceCarbon TetrachlorideHemostaticsXenobioticsacute liver failureanimal modelscoagulationhemostasisliver

Identifiers

PMID27060337
PMCPMC5091081
OpenAlexW2328891881

What OpenQuestion holds

Textmetadata
LicenceTDM
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.