Evidence map›Paper›PMID 34566967›Full record

ReviewFrontiers in immunology2021

Complement Factor D as a Strategic Target for Regulating the Alternative Complement Pathway.

Jonathan Barratt, Ilene Weitz

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06495151 (Evaluation of Serum and Peritoneal Fluid Mannose-binding Lectin Associated Serine Protease-3, Adipsin, Properdin, and Complement Factor H Levels in Endometriosis Patients), which is not on this map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
6.6field-weighted citation impact, top 2% 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.

NCT06495151 completednot on this mapstarted 2022, after this paper: background citation

Evaluation of Serum and Peritoneal Fluid Mannose-binding Lectin Associated Serine Protease-3, Adipsin, Properdin, and Complement Factor H Levels in Endometriosis Patients

TypeobservationalSponsorAnkara City Hospital BilkentRan2022 to 2022Enrolled58ConditionsEndometriosis, Complement System, Alternative Complement PathwayArmsMannose-binding lectin-associated serine protease-3 (MASP-3) Level, Adipsin Level, Properdin Level, Complement Factor H (CFH) Level, Cancer Antigen 125 (CA-125) Level
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 127 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Review
  5. Anti-Inflammatory Evaluation of Pyrazino[2,1-Pharmaceuticals (Basel, Switzerland) · 2026
    Article
  6. Article
  7. Insights into Molecular Mechanisms of Polyphenolic Compounds fromPharmaceuticals (Basel, Switzerland) · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. The 'autoimmunome' of centenarians.Journal of translational autoimmunity · 2025
    Article

17 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

2 authors at 2 institutions in 2 countries.

Jonathan BarrattDepartment of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
Ilene WeitzJane Anne Nohl Division of Hematology, University of Southern California Keck School of Medicine, Los Angeles, CA, United States.
University Hospitals of Leicester NHS Trust · GBUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system is central to first-line defense against invading pathogens. However, excessive complement activation and/or the loss of complement regulation contributes to the development of autoimmune diseases, systemic inflammation, and thrombosis. One of the three pathways of the complement system, the alternative complement pathway, plays a vital role in amplifying complement activation and pathway signaling. Complement factor D, a serine protease of this pathway that is required for the formation of C3 convertase, is the rate-limiting enzyme. In this review, we discuss the function of factor D within the alternative pathway and its implication in both healthy physiology and disease. Because the alternative pathway has a role in many diseases that are characterized by excessive or poorly mediated complement activation, this pathway is an enticing target for effective therapeutic intervention. Nonetheless, although the underlying disease mechanisms of many of these complement-driven diseases are quite well understood, some of the diseases have limited treatment options or no approved treatments at all. Therefore, in this review we explore factor D as a strategic target for advancing therapeutic control of pathological complement activation.

Indexed as

Molecular Targeted TherapyAdipose TissueAgingAntibodies, Monoclonal, HumanizedAnti-Neutrophil Cytoplasmic Antibody-Associated VasculitisAutoimmune DiseasesComplement Factor DComplement Pathway, AlternativeEnergy MetabolismGeographic AtrophyHemoglobinuria, ParoxysmalHepatocytesHumansKidney DiseasesLiverOligonucleotides, AntisenseAntibodies, Monoclonal, HumanizedCFD protein, humanComplement Factor DeculizumabOligonucleotides, AntisensepegcetacoplanPeptides, Cyclicalternative complement pathwayautoimmune diseasescomplement activationcomplement factor Dfactor Dinflammationserine protease inhibitors

Identifiers

PMID34566967
PMCPMC8458797
OpenAlexW3201532832

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.