Evidence map›Paper›PMID 39773465›Full record

ArticleeLife2025

Complement 3a receptor 1 on macrophages and Kupffer cells is not required for the pathogenesis of metabolic dysfunction-associated steatotic liver disease.

Edwin A Homan, Ankit Gilani, Alfonso Rubio-Navarro, Maya A Johnson, Odin M Schaepkens, Eric Cortada, Renan Pereira de Lima, Lisa Stoll, James C Lo

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Edwin A HomanDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.ORCID https://orcid.org/0000-0002-2923-9635
Ankit GilaniDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Alfonso Rubio-NavarroDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Maya A JohnsonDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Odin M SchaepkensDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Eric CortadaDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Renan Pereira de LimaDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
Lisa StollDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.
James C LoDivision of Cardiology, Department of Medicine, Cardiovascular Research Institute, Weill Center for Metabolic Health, Weill Cornell Medicine, New York, United States.ORCID https://orcid.org/0000-0003-0244-1670

Funding

Assessing the Impact of SARS-CoV-2 on Adipose Tissue Function and Glucose HomeostasisR01DK132879 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI James C Lo, Robert E Schwartz · 2023 to 2026
$2.8M
Dusp26 regulation of beta cell homeostasisR01DK121140 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI James C Lo · 2020 to 2026
$2.7M
An Obesity-Induced Kinase that Regulates Adipose Homeostasis and Metabolic DiseasesR01DK121844 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI LO, JAMES C · 2019 to 2023
$2.1M
Multidisciplinary Research Training in Cardiovascular DiseaseT32HL160520 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Geoffrey S Pitt, Jonathan W. Weinsaft · 2022 to 2026
$2.0M
American Diabetes Association 9-22-PDFPM-01American Heart Association 10.58275/aha.23divsup1074485.pc.gr.168377American Heart Association 908952NHLBI NIH HHS T32 HL160520NIDDK NIH HHS R01 DK121140NIDDK NIH HHS R01 DK121844NIDDK NIH HHS R01 DK132879NIH HHS 5T32HL160520NIH HHS DK121140NIH HHS DK121844NIH HHS DK132879
6 · The paper itself

Abstract

Together with obesity and type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD) is a growing global epidemic. Activation of the complement system and infiltration of macrophages has been linked to progression of metabolic liver disease. The role of complement receptors in macrophage activation and recruitment in MASLD remains poorly understood. In human and mouse,

Indexed as

Fatty LiverKupffer CellsMacrophagesMice, KnockoutReceptors, ComplementAnimalsDisease Models, AnimalHumansLiverMaleMiceMice, Inbred C57BLReceptors, G-Protein-CoupledC3a-derived anaphylatoxin receptor, mouseReceptors, ComplementReceptors, G-Protein-CoupledC3ar1fatty liver diseasehumanimmunologyinflammationkupffer cellsmacrophagesmedicinemetabolic dysfunction-associated steatotic liver diseasemousenon-alcoholic fatty liver disease

Identifiers

PMID39773465
PMCPMC11709426

What Socratic 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 Socratic graph.