Evidence map›Paper›PMID 30653682›Full record

ReviewHepatology (Baltimore, Md.)2019

The Role of Complement in Liver Injury, Regeneration, and Transplantation.

Ebbe Billmann Thorgersen, Andreas Barratt-Due, Håkon Haugaa, Morten Harboe, Søren Erik Pischke, Per H Nilsson, Tom Eirik Mollnes

Open access · hybridAbstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
15.0field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 235 citations in OpenAlex.

  1. Article
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  3. Article
  4. Risk Factors for Secondary Immunodeficiency in the Aged.The journal of allergy and clinical immunology. In practice · 2026
    Review
  5. A diagnostic dilemma in a child with Wilson's disease.Pediatric nephrology (Berlin, Germany) · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. [Scutellarin improves metabolic dysfunction-associated steatotic liver disease in rats by regulating MMP7 and LCN2].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  11. Article
  12. Article
  13. Review
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  15. Article
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  17. Review
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68 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Ebbe Billmann ThorgersenDepartment of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
Andreas Barratt-DueDepartment of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
Håkon HaugaaDivision of Emergencies and Critical Care, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Morten HarboeDepartment of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
Søren Erik PischkeDepartment of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
Per H NilssonDepartment of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
Tom Eirik MollnesDepartment of Immunology, Oslo University Hospital Rikshospitalet and University of Oslo, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NOLinnaeus University · SENorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is both an immunologically complex and a privileged organ. The innate immune system is a central player, in which the complement system emerges as a pivotal part of liver homeostasis, immune responses, and crosstalk with other effector systems in both innate and adaptive immunity. The liver produces the majority of the complement proteins and is the home of important immune cells such as Kupffer cells. Liver immune responses are delicately tuned between tolerance to many antigens flowing in from the alimentary tract, a tolerance that likely makes the liver less prone to rejection than other solid organ transplants, and reaction to local injury, systemic inflammation, and regeneration. Notably, complement is a double-edged sword as activation is detrimental by inducing inflammatory tissue damage in, for example, ischemia-reperfusion injury and transplant rejection yet is beneficial for liver tissue regeneration. Therapeutic complement inhibition is rapidly developing for routine clinical treatment of several diseases. In the liver, targeted inhibition of damaged tissue may be a rational and promising approach to avoid further tissue destruction and simultaneously preserve beneficial effects of complement in areas of proliferation. Here, we argue that complement is a key system to manipulate in the liver in several clinical settings, including liver injury and regeneration after major surgery and preservation of the organ during transplantation.

Indexed as

Liver TransplantationComplement System ProteinsGraft RejectionHumansLiverLiver RegenerationReperfusion InjuryTreatment OutcomeComplement System Proteins

Identifiers

PMID30653682
PMCPMC6771474
OpenAlexW2911087907

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.