Evidence map›Paper›PMID 42402618›Full record

ArticleNature communications2026

Sub1 contributes to heart failure with preserved ejection fraction driven by aging in mice.

Di Zhao, Ling Lin, Yufei Zhou, Jiaying Wu, Ran Xu, Linnan Li, Xiaoxue Zhang, Hong Lin, Jienan Wang, Kunming Dai and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

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.

Di ZhaoShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.ORCID http://orcid.org/0000-0001-6532-7897
Ling LinShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Yufei ZhouShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jiaying WuShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Ran XuShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Linnan LiShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Xiaoxue ZhangShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Hong LinShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Jienan WangShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Kunming DaiShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China.
Zhiwen DingInstitutes of Advanced Medical Sciences and Huaihe Hospital, Henan University, Kaifeng, Henan, China.
Pan GaoShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China. gaop11@fudan.edu.cn.ORCID http://orcid.org/0000-0003-1871-5496
Jian WuShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China. wu.jian@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0003-4259-8322
Yunzeng ZouShanghai Institute of Cardiovascular Diseases and State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University, Shanghai, China. zou.yunzeng@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0003-1310-969X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82230009National Natural Science Foundation of China (National Science Foundation of China) 82270265National Natural Science Foundation of China (National Science Foundation of China) 82430016National Natural Science Foundation of China (National Science Foundation of China) 82570295
6 · The paper itself

Abstract

Heart failure with preserved ejection fraction (HFpEF) accounts for approximately half of all heart failure cases and predominantly affects older individuals, yet effective treatments remain limited. The molecular mechanisms linking cardiac aging to HFpEF are not fully understood. Here we show that the transcriptional regulator Sub1 is upregulated in aged hearts and in mouse models of HFpEF. Cardiac overexpression of Sub1 shortens lifespan, exacerbates diastolic dysfunction, and accelerates cardiac aging, whereas Sub1 knockdown delays cardiac aging and alleviates HFpEF features, even when initiated in aged mice. Mechanistically, Sub1 interacted with TAF9b and AROS to stabilize p53 by regulating its ubiquitination and acetylation, thereby promoting cardiomyocyte senescence. Furthermore, disrupting the Sub1-p53 interaction attenuates cardiomyocyte senescence in vitro. These findings identify Sub1 as a contributor to aging-associated HFpEF and provide insight into the molecular links between cardiac aging and disease progression.

Indexed as

AgingHeart FailureStroke VolumeTranscription FactorsAcetylationAnimalsCellular SenescenceDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMyocytes, CardiacTATA-Binding Protein Associated FactorsTumor Suppressor Protein p53UbiquitinationTATA-Binding Protein Associated FactorsTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID42402618
PMCPMC13469666

What Socratic holds

Textmetadata
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.