Evidence map›Paper›PMID 42447539›Full record

ArticleJACC. Basic to translational science2026

TLR7 Inhibition Limits Ischemic Cardiac Injury by Disrupting ITGAM-Dependent Immune-Endothelial Interactions.

Yijia Li, Yang Yang, Chanhee Park, Boyang Ren, Ruoxing Li, Amol Shetty, Brittney Williams, Ziyi Li, Lin Zou, Wei Chao

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 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

5 · Who and what money

Authors and funding

10 authors.

Yijia LiTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Yang YangTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Chanhee ParkTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Boyang RenTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Ruoxing LiDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Amol ShettyInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Brittney WilliamsTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Ziyi LiDepartment of Biostatistics, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Lin ZouTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Wei ChaoTranslational Research Program, Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, Baltimore, Maryland, USA. Electronic address: wchao@som.umaryland.edu.

Funding

Extracellular miRNAs, innate immunity, and critical illnessR35GM140822 · UNIVERSITY OF MARYLAND BALTIMORE · 2025 to 2025
$386k
NIGMS NIH HHS R35 GM140822
6 · The paper itself

Abstract

Percutaneous coronary intervention, such as stenting, restores coronary perfusion after myocardial ischemia but also induces ischemia-reperfusion (I/R) injury, in part driven by innate immune activation. Here, we identified Toll-like receptor 7 (TLR7), an endosomal sensor of single-stranded RNA, as a key mediator of postischemic inflammation. Genetic deletion or pharmacologic inhibition of TLR7 with enpatoran reduced inflammation and myocardial infarction (MI) size and improved cardiac function 24 hours after I/R in mice. Single-nucleus RNA sequencing demonstrated coordinated induction of TLR7-responsive inflammatory endothelial and myeloid cell programs, including increased endothelial ITGAM expression and leukocyte adhesion. TLR7/8 activation promoted ITGAM-dependent endothelial-leukocyte interactions under shear stress, whereas ITGAM blockade reduced immune cell infiltration and limited MI injury. These findings identify the TLR7-ITGAM signaling axis as a central driver of endothelial-leukocyte crosstalk in myocardial I/R injury and support TLR7 inhibition as a promising therapeutic strategy to mitigate ischemic MI after percutaneous coronary intervention.

Indexed as

endothelial-leukocyte crosstalkenpatoranICAM1-ITGAMmyocardial ischemia-reperfusion injurysingle-nucleus RNA sequencingTLR7/8

Identifiers

PMID42447539
PMCPMC13382253

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.