Evidence map›Paper›PMID 41467029›Full record

ArticleFundamental research2025

Myocardial infarction creates a critical time window for AAV-based cardiac gene transfer.

Gonglie Chen, Yueyang Zhang, Zhanzhao Liu, Jingdong Wu, Zhan Chen, Luzi Yang, Junxia Zhang, Yufei Wu, Jiting Li, Baochen Bai and 4 more

Abstract read
In one paragraph

Article in Fundamental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Cardiomyocyte-Derived USP20 Attenuates Diabetic Cardiomyopathy by Facilitating the Degradation of STING and Mitigating STING-Mediated Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. 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

14 authors.

Gonglie ChenSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Yueyang ZhangSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Zhanzhao LiuSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Jingdong WuCenter for Life Sciences, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing 100871, China.
Zhan ChenSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Luzi YangSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Junxia ZhangDepartment of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.
Yufei WuSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Jiting LiSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Baochen BaiDepartment of Cardiology, Peking University People's Hospital, Beijing 100044, China.
Zhengyuan LvSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Fei GaoDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Erdan DongSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.
Yuxuan GuoSchool of Basic Medical Sciences and Institute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Beijing 100191, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Approaches to enhance adeno-associated virus (AAV)-based cardiac gene transfer are the key to successful cardiac gene therapy, but factors influencing AAV transduction remain poorly investigated. This study showed that myocardial infarction (MI) enhanced cardiac AAV transduction, peaking at the third day post-MI in mice. The excessive AAV enrichment at the border zone is due to local vascular permeabilization and cardiomyocyte metabolic remodeling, which is independent of AAV dosage, serotypes and promoters. This effect was harnessed to boost cardiac base editing and improve the outcome of gene therapy for MI in mice. Thus, heart disease itself is a non-negligible factor that alters AAV-based cardiac gene transfer, which provides a new inroad to develop approaches to enhance cardiac gene therapy.

Indexed as

Adeno-associated virusGene deliveryGene editingGene therapyMyocardial infarction

Identifiers

PMID41467029
PMCPMC12744679

What OpenQuestion 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 OpenQuestion graph.