Evidence map›Paper›PMID 27959629›Full record

ReviewAnnual review of pathology2017

Complement Dysregulation and Disease: Insights from Contemporary Genetics.

M Kathryn Liszewski, Anuja Java, Elizabeth C Schramm, John P Atkinson

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Review
  6. Article
  7. Inside job: Roles of intracellular C3.The Journal of allergy and clinical immunology · 2025
    Review
  8. Article
  9. Post-transplant Thrombotic Microangiopathy.Journal of the American Society of Nephrology : JASN · 2025
    Review
  10. Article
  11. Review
  12. Atypical hemolytic uremic syndrome: diagnosis, management, and discontinuation of therapy.Hematology. American Society of Hematology. Education Program · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Rare DysfunctionalOphthalmology science · 2023
    Article
  20. 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

4 authors at 1 institution in 1 country.

M Kathryn LiszewskiDivision of Rheumatology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110; email: j.p.atkinson@wustl.edu.
Anuja JavaDivision of Nephrology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
Elizabeth C SchrammSerion Inc., St. Louis, Missouri 63108.
John P AtkinsonDivision of Rheumatology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110; email: j.p.atkinson@wustl.edu.
Washington University in St. Louis · US

Funding

Translational Research Skills Development CoreU54HL112303 · NHLBI · WASHINGTON UNIVERSITY · PI SADLER, J EVAN · 2012 to 2016
$8.8M
RENAL DISEASET32DK007126 · NIDDK · WASHINGTON UNIVERSITY · PI HUMPHREYS, BENJAMIN D. · 1986 to 2022
$5.2M
INTRACELLULAR C3 PROTEINS: SOURCE, COMPOSITION, TRAFFICKING AND FUNCTIONR01GM099111 · NIGMS · WASHINGTON UNIVERSITY · PI ATKINSON, JOHN · 2011 to 2019
$2.7M
NHLBI NIH HHS U54 HL112303NIDDK NIH HHS T32 DK007126NIGMS NIH HHS R01 GM099111
6 · The paper itself

Abstract

The vertebrate complement system consists of sequentially interacting proteins that provide for a rapid and powerful host defense. Nearly 60 proteins comprise three activation pathways (classical, alternative, and lectin) and a terminal cytolytic pathway common to all. Attesting to its potency, nearly half of the system's components are engaged in its regulation. An emerging theme over the past decade is that variations in these inhibitors predispose to two scourges of modern humans. One, occurring most often in childhood, is a rare but deadly thrombomicroangiopathy called atypical hemolytic uremic syndrome. The other, age-related macular degeneration, is the most common form of blindness in the elderly. Their seemingly unrelated clinical presentations and pathologies share the common theme of overactivity of the complement system's alternative pathway. This review summarizes insights gained from contemporary genetics for understanding how dysregulation of this powerful innate immune system leads to these human diseases.

Indexed as

Atypical Hemolytic Uremic SyndromeComplement Pathway, AlternativeComplement System ProteinsGenotypeHumansMacular DegenerationComplement System Proteinsage-related macular degenerationalternative complement pathwayatypical hemolytic uremic syndromeC3C3 glomerulopathiesCD46factor Bfactor Hfactor I

Identifiers

PMID27959629
PMCPMC6020056
OpenAlexW2412863605

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.