Evidence map›Paper›PMID 24970127›Full record

ArticleBiomolecules2012

Factor h: a complement regulator in health and disease, and a mediator of cellular interactions.

Anne Kopp, Mario Hebecker, Eliška Svobodová, Mihály Józsi

Open access · goldAbstract read
In one paragraph

Article in Biomolecules, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

82 citing papers in PubMed, 155 citations in OpenAlex.

  1. Article
  2. Review
  3. Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026
    Review
  4. Review
  5. Redox modulation of the complement cascade contributes to synapse loss in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Molecular Analysis ofPathogens (Basel, Switzerland) · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Article

22 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

4 authors at 1 institution in 1 country.

Anne KoppJunior Research Group Cellular Immunobiology, Leibniz Institute for Natural Product Research and Infection Biology, Jena 07745, Germany. anne.braunschweig@hki-jena.de.
Mario HebeckerJunior Research Group Cellular Immunobiology, Leibniz Institute for Natural Product Research and Infection Biology, Jena 07745, Germany. mario.hebecker@hki-jena.de.
Eliška SvobodováJunior Research Group Cellular Immunobiology, Leibniz Institute for Natural Product Research and Infection Biology, Jena 07745, Germany. eliska.svobodova@hki-jena.de.
Mihály JózsiJunior Research Group Cellular Immunobiology, Leibniz Institute for Natural Product Research and Infection Biology, Jena 07745, Germany. mihaly.jozsi@gmx.net.
Leibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement is an essential part of innate immunity as it participates in host defense against infections, disposal of cellular debris and apoptotic cells, inflammatory processes and modulation of adaptive immune responses. Several soluble and membrane-bound regulators protect the host from the potentially deleterious effects of uncontrolled and misdirected complement activation. Factor H is a major soluble regulator of the alternative complement pathway, but it can also bind to host cells and tissues, protecting them from complement attack. Interactions of factor H with various endogenous ligands, such as pentraxins, extracellular matrix proteins and DNA are important in limiting local complement-mediated inflammation. Impaired regulatory as well as ligand and cell recognition functions of factor H, caused by mutations or autoantibodies, are associated with the kidney diseases: atypical hemolytic uremic syndrome and dense deposit disease and the eye disorder: age-related macular degeneration. In addition, factor H binds to receptors on host cells and is involved in adhesion, phagocytosis and modulation of cell activation. In this review we discuss current concepts on the physiological and pathophysiological roles of factor H in light of new data and recent developments in our understanding of the versatile roles of factor H as an inhibitor of complement activation and inflammation, as well as a mediator of cellular interactions. A detailed knowledge of the functions of factor H in health and disease is expected to unravel novel therapeutic intervention possibilities and to facilitate the development or improvement of therapies.

Identifiers

PMID24970127
PMCPMC4030870
OpenAlexW2071731444

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.