Evidence map›Paper›PMID 32390699›Full record

ReviewWorld journal of gastroenterology2020

Regulation of macrophage activation in the liver after acute injury: Role of the fibrinolytic system.

Katherine Roth, Jenna Strickland, Bryan L Copple

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. [Therapeutic plasma exchange in the pediatric intensive care unit: a single-center retrospective study].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022
    Article
  13. Recovered Hepatocytes Promote Macrophage Apoptosis Through CXCR4 After Acetaminophen-Induced Liver Injury in Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Article
  14. Article
  15. Review
  16. Article
  17. [Application of double plasma molecular adsorption system in children with acute liver failure].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021
    Article
  18. Review
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.

Katherine RothDepartment of Pharmacology and Toxicology, Institute for Integrative Toxicology, Michigan State University, East Lansing, MI 48824, United States.
Jenna StricklandDepartment of Pharmacology and Toxicology, Institute for Integrative Toxicology, Michigan State University, East Lansing, MI 48824, United States.
Bryan L CoppleDepartment of Pharmacology and Toxicology, Institute for Integrative Toxicology, Michigan State University, East Lansing, MI 48824, United States. copple@msu.edu.
Michigan State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver functions, in part, to prevent exposure of the body to potentially harmful substances ingested in the diet. While it is highly efficient at accomplishing this, it is frequently prone to liver injury due to the biotransformation of xenobiotics into toxic metabolites. To counter this injury, the liver has evolved a unique capacity to rapidly and efficiently repair itself. Successful resolution of acute liver injury relies on hepatic macrophage populations that orchestrate the reparative response. After injury, Kupffer cells, the resident macrophages of the liver, become activated and secrete proinflammatory cytokines. These cytokines recruit other immune cells, including monocyte-derived macrophages, to the liver where they contribute to the repair process. Monocyte-derived macrophages traffic into the necrotic foci where they rapidly phagocytose dead cell debris. Simultaneous with this process, these cells change phenotype from a proinflammatory macrophage to a pro-restorative macrophage that produce pro-mitogenic growth factors and anti-inflammatory cytokines. Ultimately this process triggers resolution of inflammation, and along with proliferation of other hepatic cells, restores the liver architecture and function. While the mechanisms regulating specific macrophage functions during repair remain to be elucidated, recent studies indicate a key role for the fibrinolytic system in coordinating macrophage function during repair. In this review, we will highlight the function and role of hepatic macrophages in repair after acute liver injury, and will discuss the role of the fibrinolytic enzyme, plasmin, in regulation of these various processes.

Indexed as

Macrophage ActivationAcetaminophenAnimalsCell ProliferationChemical and Drug Induced Liver InjuryCytokinesDisease Models, AnimalFibrinolysisHepatic Stellate CellsHumansInflammation MediatorsKupffer CellsLiverLiver RegenerationAcetaminophenCytokinesInflammation MediatorsAcetaminophenLiver injuryLiver repairMacrophagePlasmin

Identifiers

PMID32390699
PMCPMC7201151
OpenAlexW3022518324

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.