Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing 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.
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
10 authors.
Xun WuCardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, 10032, USA. xw2698@cumc.columbia.edu.ORCID http://orcid.org/0000-0002-0742-7459
Ziyi WangCardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Katherine R CroceDepartment of Neurology, Columbia University, New York, NY, 10032, USA.
Fang LiCardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Jian CuiCardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, 10032, USA.
Vivette D D'AgatiDepartment of Pathology and Cell Biology, Columbia University, New York, NY, 10032, USA.
Ira TabasDepartment of Pathology and Cell Biology, Columbia University, New York, NY, 10032, USA.
Ai YamamotoDepartment of Neurology, Columbia University, New York, NY, 10032, USA.
Hanrui ZhangCardiometabolic Genomics Program, Division of Cardiology, Department of Medicine, Columbia University Irving Medical Center, New York, NY, 10032, USA. hz2418@cumc.columbia.edu.ORCID http://orcid.org/0000-0001-8655-938X
Funding
Tumor Biology and Microenvironment ProgramP30CA013696 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI Parisa Tehranifar · 1985 to 2026
$115.3M
Clinical and Translational Science AwardUL1TR001873 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REILLY, MUREDACH P · 2016 to 2025
$99.0M
Translational Biomarker Analytical Core (TBAC)P30DK063608 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DOMENICO ACCILI · 2003 to 2026
$36.7M
Mouse and Human Atherosclerotic TissueP01HL172741 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Hanrui Zhang · 2024 to 2026
$9.5M
A Mechanistic and Translational Research Program Linking Impaired Resolution, Defective Efferocytosis, and Clonal Hematopoiesis to the Formation of Clinically Dangerous Atherosclerotic PlaquesR35HL145228 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2019 to 2025
$6.8M
Modulating selective autophagy to modify Huntington's diseaseR01NS077111 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Ai Yamamoto · 2012 to 2026
$4.3M
Selective autophagy in Parkinson'sdiseaseR01NS101663 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Ai Yamamoto · 2018 to 2026
$3.1M
Integrative genomic and functional genomic studies to connect variant to function for CAD GWAS lociR01HL168174 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Wei Li, EDOARDO MARCORA · 2023 to 2026
$3.1M
Discovering Wdfy3 as a novel regulator of macrophage efferocytosis by genome-wide CRISPR screenR01HL151611 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ZHANG, HANRUI · 2020 to 2024
$3.0M
Calcium signaling and autophagy defects in Alzheimer's disease neuronsR01AG090542 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Ai Yamamoto · 2025 to 2026
$1.5M
Finding and pushing the limits of macrophage efferocytosis in atherosclerosisR35HL177389 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Hanrui Zhang · 2025 to 2026
$1.3M
BD Biosciences InfluxS10OD020056 · OD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SNOECK, HANS-WILLEM E · 2015 to 2015
$600k
American Heart Association (American Heart Association, Inc.) 23CDA1052177American Heart Association (American Heart Association, Inc.) 25CDA1451366NCATS NIH HHS UL1 TR001873NCI NIH HHS P30 CA013696NCRR NIH HHS S10 RR027050NHLBI NIH HHS P01 HL172741NHLBI NIH HHS R01 HL151611NHLBI NIH HHS R01 HL168174NHLBI NIH HHS R35 HL145228NHLBI NIH HHS R35 HL177389NIA NIH HHS R01 AG090542NIDDK NIH HHS P30 DK063608NIH HHS S10 OD020056NINDS NIH HHS R01 NS077111NINDS NIH HHS R01 NS101663U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) P01HL172741U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL151611U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R01HL168174U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R35HL177389
6 · The paper itself
Abstract
Efficient efferocytosis is crucial for immune homeostasis. Conversely, excessive apoptotic cell (AC) death and impaired macrophage efferocytosis lead to autoantigen release, autoantibody production, and immune activation. It is unclear whether immunogenic autoantigens from impaired clearance are the sole cause of autoimmunity or if AC efferocytosis directly alters macrophage function, affecting T cell activation and amplifying autoimmunity. Our prior work identified WDFY3 as essential for macrophage efferocytosis. Here, we demonstrate that myeloid Wdfy3 knockout exacerbates autoimmunity in young mice receiving systemic AC injections and middle-aged mice developing autoreactivity. Mechanistically, myeloid Wdfy3 deletion impairs efferocytosis, increasing autoantigen availability, and augments MHC-II-mediated antigen presentation and cytokine dysregulation, thereby promoting CD4
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.
Macrophage WDFY3 mitigates autoimmunity by enhancing efferocytosis and suppressing T cell activation in mice. · full record | OpenQuestion