Evidence map›Paper›PMID 37055581›Full record

ReviewNature reviews. Nephrology2023

Complosome - the intracellular complement system.

Erin E West, Claudia Kemper

Open access · bronzeAbstract readReview
In one paragraph

Review in Nature reviews. Nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
37.5field-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

149 citing papers in PubMed, 224 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Innate immunity: current understandings and future perspectives.Signal transduction and targeted therapy · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Peripheral complement C4 protein in schizophrenia: Association with gene copy number and immune cell subtypes.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  17. Review
  18. Article
  19. Complement activation in kidney transplantation.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2026
    Review
  20. Article

89 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 1 institution in 1 country.

Erin E WestNational Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Complement and Inflammation Research Section (CIRS), Bethesda, MD, USA.ORCID 0000-0002-7103-8394
Claudia KemperNational Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Complement and Inflammation Research Section (CIRS), Bethesda, MD, USA. claudia.kemper@nih.gov.ORCID 0000-0003-4196-1417
National Institutes of Health · US

Funding

The role of the intracellular complement system - the complosome - in Th1 biologyZIAHL006223 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI KEMPER, CLAUDIA · 2017 to 2025
$16.9M
Intramural NIH HHS ZIA HL006223
6 · The paper itself

Abstract

The complement system is a recognized pillar of host defence against infection and noxious self-derived antigens. Complement is traditionally known as a serum-effective system, whereby the liver expresses and secretes most complement components, which participate in the detection of bloodborne pathogens and drive an inflammatory reaction to safely remove the microbial or antigenic threat. However, perturbations in normal complement function can cause severe disease and, for reasons that are currently not fully understood, the kidney is particularly vulnerable to dysregulated complement activity. Novel insights into complement biology have identified cell-autonomous and intracellularly active complement - the complosome - as an unexpected central orchestrator of normal cell physiology. For example, the complosome controls mitochondrial activity, glycolysis, oxidative phosphorylation, cell survival and gene regulation in innate and adaptive immune cells, and in non-immune cells, such as fibroblasts and endothelial and epithelial cells. These unanticipated complosome contributions to basic cell physiological pathways make it a novel and central player in the control of cell homeostasis and effector responses. This discovery, together with the realization that an increasing number of human diseases involve complement perturbations, has renewed interest in the complement system and its therapeutic targeting. Here, we summarize the current knowledge about the complosome across healthy cells and tissues, highlight contributions from dysregulated complosome activities to human disease and discuss potential therapeutic implications.

Indexed as

Complement System ProteinsInflammationHumansKidneyComplement System Proteins

Identifiers

PMID37055581
PMCPMC10100629
OpenAlexW4365449961

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.