Evidence map›Paper›PMID 32194049›Full record

ReviewThe American journal of pathology2020

Complement Membrane Attack Complex: New Roles, Mechanisms of Action, and Therapeutic Targets.

Catherine B Xie, Dan Jane-Wit, Jordan S Pober

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
8.4field-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

136 citing papers in PubMed, 206 citations in OpenAlex.

  1. Trial
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  8. Article
  9. Proteomic Profiling of Complement Components in Glomerular Disease.Laboratory investigation; a journal of technical methods and pathology · 2026
    Article
  10. Article
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  13. Review
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76 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

3 authors at 1 institution in 1 country.

Catherine B XieDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut.
Dan Jane-WitDivision of Cardiovascular Medicine, Yale University School of Medicine, New Haven, Connecticut.
Jordan S PoberDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut. Electronic address: jordan.pober@yale.edu.
Yale University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Optimizing Therapeutic Revascularization by Endothelial Cell TransplantationR01HL085416 · NHLBI · YALE UNIVERSITY · PI POBER, JORDAN S, SALTZMAN, W. MARK · 2006 to 2019
$5.9M
THE ROLE OF ZFYVE21 IN CEREBRAL AMYLOID ANGIOPATHY IN ALZHEIMER'S DISEASER01HL141137 · NHLBI · YALE UNIVERSITY · PI JANE-WIT, DANIEL · 2018 to 2022
$2.6M
Ex Vivo Nanoparticle Drug Delivery Targeted to Human Renal Allograft EndotheliumU01AI132895 · NIAID · YALE UNIVERSITY · PI POBER, JORDAN S, SALTZMAN, W. MARK · 2017 to 2021
$2.2M
Complement Induces Inflammasome Assembly in Human Endothelium: Mechanisms and Consequences for Graft RejectionF30AI138473 · NIAID · YALE UNIVERSITY · PI XIE, CATHERINE BINGCHAN · 2018 to 2021
$140k
NHLBI NIH HHS R01 HL085416NHLBI NIH HHS R01 HL141137NIAID NIH HHS F30 AI138473NIAID NIH HHS U01 AI132895NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

The complement membrane attack complex (MAC) is classically known as a cytolytic effector of innate and adaptive immunity that forms pores in the plasma membrane of pathogens or targeted cells, leading to osmolysis. Nucleated cells resist MAC-mediated cytolysis by expression of inhibitors that block MAC assembly or by rapid removal of MAC through endocytosis or shedding. In the absence of lysis, MAC may induce intracellular signaling and cell activation, responses implicated in a variety of autoimmune, inflammatory, and transplant disease settings. New discoveries into the structure and biophysical properties of MAC revealed heterogeneous MAC precursors and conformations that provide insights into MAC function. In addition, new mechanisms of MAC-mediated signaling and its contribution to disease pathogenesis have recently come to light. MAC-activated cells have been found to express proinflammatory proteins-often through NF-κB-dependent transcription, assemble inflammasomes, enabling processing, and facilitate secretion of IL-1β and IL-18, as well as other signaling pathways. These recent insights into the mechanisms of action of MAC provide an updated framework to therapeutic approaches that can target MAC assembly, signaling, and proinflammatory effects in various complement-mediated diseases.

Indexed as

Adaptive ImmunityAnimalsComplement ActivationComplement Membrane Attack ComplexHumansImmunity, InnateInterleukinsNF-kappa BSignal TransductionComplement Membrane Attack ComplexInterleukinsNF-kappa B

Identifiers

PMID32194049
PMCPMC7280757
OpenAlexW3012469351

What OpenQuestion holds

Textmetadata
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.