Evidence map›Paper›PMID 41882094›Full record

ArticleActa pharmacologica Sinica2026

Non-telomeric function deficiency of TERT enhances pressure overload-induced mouse cardiac remodeling by activation of CNBP-mediated THBS3/ITGB1 pathway.

Ying-Ying Liu, Ying-Chao Wang, Wen-Yan Gong, Hui Luo, Jing-Hua Yuan, Zhen Chen, Xiao-Ling Xu, Jing Yang, Yu-Sheng Cong, Xing-Wei Zhang and 1 more

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Article in Acta pharmacologica Sinica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

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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

11 authors.

Ying-Ying LiuBasic Laboratory of Cardiovascular Disease, Institute of Translational Medicine, Affiliated Hospital of Hangzhou Normal University, Hangzhou, 310015, China.
Ying-Chao WangInnovation Institute for Artificial Intelligence in Medicine, Zhejiang University, Hangzhou, 310020, China.
Wen-Yan GongHangzhou Institute of Cardiovascular Disease, Hangzhou, 310015, China.
Hui LuoHangzhou Institute of Cardiovascular Disease, Hangzhou, 310015, China.
Jing-Hua YuanHangzhou Institute of Cardiovascular Disease, Hangzhou, 310015, China.
Zhen ChenBasic Laboratory of Cardiovascular Disease, Institute of Translational Medicine, Affiliated Hospital of Hangzhou Normal University, Hangzhou, 310015, China.
Xiao-Ling XuHangzhou Institute of Cardiovascular Disease, Hangzhou, 310015, China.
Jing YangKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 31112, China.
Yu-Sheng CongKey Laboratory of Aging and Cancer Biology of Zhejiang Province, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 31112, China.
Xing-Wei ZhangHangzhou Institute of Cardiovascular Disease, Hangzhou, 310015, China.
Qi-Bin JiaoBasic Laboratory of Cardiovascular Disease, Institute of Translational Medicine, Affiliated Hospital of Hangzhou Normal University, Hangzhou, 310015, China. 20130012@hznu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies show that telomerase reverse transcriptase (TERT) possesses important new biological functions in gene transcription regulation, signal transduction, tumorigenesis, vascular development and mitochondrial DNA protection independent of the maintenance of telomere length. In this study we investigated the role and mechanisms of TERT in regulating the gene expression and signal transduction during pressure overload-induced cardiac remodeling. The first-generation TERT knockout (Tert

Indexed as

TelomeraseVentricular RemodelingAnimalsCardiomegalyFibrosisMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacRatsSignal TransductionTelomeraseTert protein, mousecardiac fibrosiscardiac remodelingCNBPnon-telomeric functionpressure overloadTERT

Identifiers

PMID41882094
PMCPMC13389254

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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.