Evidence map›Paper›PMID 41965774›Full record

ArticleJournal of nanobiotechnology2026

Therapeutic potential of ADAR1-regulated macrophage exosomes for improving myocardial damage in septic cardiomyopathy.

Linxiao Wang, Shanshou Liu, Xianqi Wang, Huirong Wu, Xiaojun Zhao, Dan Wu, Qianmei Wang, Peiwen Wang, Yanan Xu, Kuo Shen and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Linxiao Wang *Department of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Shanshou Liu *Department of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Xianqi Wang *Department of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Huirong WuDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Xiaojun ZhaoDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Dan WuDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Qianmei WangDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Peiwen WangDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Yanan XuDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China.
Kuo ShenDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China. shenkuodoc@fmmu.edu.cn.
Juzheng YuanDepartment of General Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China. yuanjz0616@163.com.
Junjie LiDepartment of Emergency, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, Shaanxi, China. lijunjie@fmmu.edu.cn.

Funding

the Key Research and Development Program of Shaanxi Province 2025JC-QYCX-083the Key Research and Development Program of Shaanxi Province 2025JC-YBQN-1295the National Natural Science Foundation of China 82572467Youth Science Fund Project 82502995
6 · The paper itself

Abstract

backgroundSepsis-induced cardiomyopathy (SICM) is a critical cardiovascular complication characterized by cardiac dysfunction and high mortality. The molecular mechanisms that underlie SICM remain elusive, and effective therapies are limited.

resultsHere, we report a pivotal role for adenosine deaminases acting on RNA-1 (ADAR1) in modulating macrophage polarization and exosome-mediated intercellular communication, which ameliorates myocardial damage in SICM. We determined that ADAR1 overexpression in macrophages promotes an anti-inflammatory M2 phenotype, reduces myocardial inflammation, and inhibits cardiomyocyte apoptosis in a murine model of sepsis. Mechanistically, ADAR1 regulates the level of microRNA-122 (miR-122) in macrophage-derived exosomes. Exosomal miR-122 targets X-linked inhibitor of apoptosis protein (XIAP), modulating cardiomyocyte survival.

conclusionsOur study reveals a novel ADAR1-miR-122-XIAP axis in macrophage exosomes that protects against sepsis-induced myocardial injury, offering a potential disease modulation strategy for SICM.

Indexed as

Adenosine DeaminaseCardiomyopathiesExosomesMacrophagesSepsisAnimalsApoptosisHumansMaleMiceMice, Inbred C57BLMicroRNAsMyocardiumMyocytes, CardiacRAW 264.7 CellsADAR1 protein, mouseAdenosine DeaminaseMicroRNAsADAR1ApoptosisCardiomyopathyExosomesMicroRNASepsis

Identifiers

PMID41965774
PMCPMC13200382

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.