Evidence mapPaperPMID 42412640Full record

ArticleAmerican journal of physiology. Renal physiology2026

Deletion of decay-accelerating factor in kidney tubular cells mitigates kidney fibrosis in aristolochic acid nephropathy.

Samuel Mon-Wei Yu, Emily King, Sari Khleif, Paolo Cravedi

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Samuel Mon-Wei YuNephrology Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States.ORCID 0000-0003-3554-5599
Emily KingNephrology Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States.
Sari KhleifNephrology Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States.
Paolo CravediNephrology Division, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, United States.

Funding

Central Hub for Kidney Precision MedicineU24DK114886 · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · 2025 to 2025
$4.2M
KPMP Kidney Mapping and Atlas Project (KMAP)U01DK133090 · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2025 to 2025
$2.3M
Integrated spatial interrogation of cellular and molecular signatures of human kidney diseaseU01DK114923 · INDIANA UNIVERSITY INDIANAPOLIS · 2025 to 2025
$1.1M
Single cell multiomic and spatial atlas of acute and chronic kidney injuryU01DK114933 · WASHINGTON UNIVERSITY · 2025 to 2025
$1.0M
Spatial Multi-Omics to Profile Metabolic Pathways for Kidney DiseaseU01DK114920 · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2025 to 2025
$824k
Boston Chronic Kidney Disease Research Biopsy CenterU01DK133092 · BOSTON MEDICAL CENTER · 2025 to 2025
$800k
Multimodal Imaging Mass Spectrometry and Spatial Omics for the Human KidneyU01DK133766 · VANDERBILT UNIVERSITY · 2025 to 2025
$729k
University of Illinois at Chicago KPMP CKD Recruitment SiteU01DK133081 · UNIVERSITY OF ILLINOIS AT CHICAGO · 2025 to 2025
$630k
PREcision Medicine through IntErrogation of Rna in the kidnEy (PREMIERE)U01DK114907 · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2025 to 2025
$627k
AKI Matched Phenotype Linked Evaluation with Tissue (AMPLE-Tissue)U01DK114866 · JOHNS HOPKINS UNIVERSITY · 2025 to 2025
$550k
Minnesota Precision Medicine CKD & Resilient Diabetes Recruiting Site: Engagement, Enrollment & EthicsU01DK133097 · UNIVERSITY OF MINNESOTA · 2025 to 2025
$500k
Cleveland Precision Medicine Chronic Kidney Disease CohortU01DK114908 · CLEVELAND CLINIC LERNER COM-CWRU · 2025 to 2025
$491k
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK132501-01A1HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) DK119431NIDDK NIH HHS K08 DK132501NIDDK NIH HHS U01 DK114866NIDDK NIH HHS U01 DK114907NIDDK NIH HHS U01 DK114908NIDDK NIH HHS U01 DK114920NIDDK NIH HHS U01 DK114923NIDDK NIH HHS U01 DK114933NIDDK NIH HHS U01 DK133081NIDDK NIH HHS U01 DK133090NIDDK NIH HHS U01 DK133091NIDDK NIH HHS U01 DK133092NIDDK NIH HHS U01 DK133093NIDDK NIH HHS U01 DK133095NIDDK NIH HHS U01 DK133097NIDDK NIH HHS U01 DK133113NIDDK NIH HHS U01 DK133766NIDDK NIH HHS U01 DK133768NIDDK NIH HHS U24 DK114886NIDDK NIH HHS UH3 DK114861NIDDK NIH HHS UH3 DK114915NIDDK NIH HHS UH3 DK114926NIDDK NIH HHS UH3 DK114937
6 · The paper itself

Abstract

Local complement activation is increasingly recognized as a key contributor to kidney injury and fibrosis, although protective roles have also been described. The decay-accelerating factor (DAF, CD55) is a membrane-bound complement regulator that disrupts C3 and C5 convertases and limits complement activation on the cell surface. Although renal tubular epithelial cells (RTECs) are a major source of complement components in the kidney, the role of DAF in tubular injury and repair remains unclear. Here, we investigated the function of DAF in kidney tubules using global and tubule-specific DAF knockout mice in a model of aristolochic acid nephropathy (AAN). Publicly available single-cell and single-nucleus transcriptomic datasets revealed high

Indexed as

Aristolochic AcidsCD55 AntigensEpithelial CellsKidney DiseasesKidney TubulesKidney Tubules, ProximalAnimalsCells, CulturedComplement ActivationComplement C3Disease Models, AnimalFibrosisMaleMiceMice, Inbred C57BLMice, Knockoutaristolochic acid IAristolochic AcidsCD55 AntigensComplement C3decay-accelerating factor 1, mouseacute kidney injurycomplementdecay-accelerating factorkidney fibrosiskidney tubule

Identifiers

PMID42412640
PMCPMC13472027

What Socratic 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 Socratic graph.