Evidence map›Paper›PMID 41806656›Full record

ArticleEBioMedicine2026

Modified hTERT treatment ameliorates pressure overload-induced heart failure.

Yinlong Zhao, Xiaolu Bao, Weiyao Xiong, Xin Wan, Qingying Yu, Teng Wang, Andrew C H Chang, Yangyang Liu, Yanqiu Wang, Ching Shang and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 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
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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

17 authors.

Yinlong ZhaoDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Xiaolu BaoDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Weiyao XiongDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Xin WanDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Qingying YuJuvensis Therapeutics, Shanghai, China.
Teng WangDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Andrew C H ChangDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Yangyang LiuJuvensis Therapeutics, Shanghai, China.
Yanqiu WangJuvensis Therapeutics, Shanghai, China.
Ching ShangDivision of Cardiology, Department of Medicine, Stanford University, Palo Alto, CA, USA.
Min WuDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China.
Euan A AshleyDivision of Cardiology, Department of Medicine, Stanford University, Palo Alto, CA, USA.
Ming LeiShanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China.
Junfeng ZhangDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China. Electronic address: zhangjf1222@sjtu.edu.cn.
Yueheng WuDepartment of Cardiovascular Surgery, Guangdong Provincial Key Laboratory of South China Structural Heart Disease, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong, China. Electronic address: wuyueheng@gdph.org.cn.
Wei HanDepartment of Heart Failure, Heart Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China. Electronic address: 2100504@tongue.edu.cn.
Alex C Y ChangDepartment of Cardiology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China; Shanghai Institute of Precision Medicine, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200125, China. Electronic address: alexchang@shsmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHeart failure (HF) is a currently incurable disorder that increases the risk for stroke and sudden cardiac death. Shortened telomeres have been linked to the development of cardiomyocyte abnormalities and dysfunction, and telomere reprotection has become a favourable strategy for designing novel heart failure therapies. This study aims to design a pan-HF gene therapy where modified human telomerase expression is driven by cardiac troponin promoter and to evaluate cardiac protection.

methodsTelomere shortening was determined in cardiomyocytes from Macaca fascicularis (cynomolgus monkey) and patients with HF by quantitative fluorescence in situ hybridisation (Q-FISH) assays. We bioengineered a catalytic inactivation and nuclear retaining modified human TERT (telomerase reverse transcriptase) gene therapy (AAV9-modhTERT

findingsAAV9-modhTERT

interpretationWe provide evidence that telomere re-protection confers cardiac protection and may serve as a potential gene therapeutic option for treating heart failure.

fundingThis research was supported by the National Natural Science Foundation of China (82070248, 82300282, 82300476), the Program for Professor of Special Appointment (Eastern Scholar) at Shanghai Institutions of Higher Learning (0900000024), 2023 Shanghai Action Plan for Promoting Scientific and Technological Innovation and Industrial Development of Gene Therapy (23J11900600).

Indexed as

Genetic TherapyHeart FailureTelomeraseAnimalsDisease Models, AnimalGenetic VectorsHumansInduced Pluripotent Stem CellsMacaca fascicularisMaleMiceMyocytes, CardiacTelomereTelomere ShorteningTelomeraseTERT protein, humanDNA damage responseHeart failurehiPSC-CMsMitochondriaTelomere

Identifiers

PMID41806656
PMCPMC12993239

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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.