Evidence map›Paper›PMID 41322586›Full record

ArticleACS omega2025

Global Profiling of the Proteome and Acetylome in Mice with Abdominal Aortic Aneurysms.

Luyao Zhang, Bo Yang, Tao Ding, Yaling Zhao, Yehong Yang, Xiaoyue Tang, Yue Wu, Qiaochu Wang, Zhiyi Zhang, Chunmei Shi and 4 more

Abstract read
In one paragraph

Article in ACS omega, 2025. 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.

Luyao ZhangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Bo YangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Tao DingState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Yaling ZhaoDepartment of Blood Transfusion, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China.
Yehong YangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Xiaoyue TangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Yue WuState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Qiaochu WangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Zhiyi ZhangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Chunmei ShiState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Rong HanState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Xutong ZhangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Jiangfeng LiuState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.
Juntao YangState Key Laboratory of Common Mechanism Research for Major Diseases, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100005, China.ORCID https://orcid.org/0000-0003-1180-391X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abdominal aortic aneurysm (AAA) is a fatal vascular disease with a high rupture risk, and current treatments rely mainly on surgery. Pharmacological therapies are limited due to an incomplete understanding of disease mechanisms. This study aimed to identify potential targets for pharmacological intervention in AAA using a mouse model, focusing on proteomic and acetylomic alterations in aortic tissues. We successfully established a mouse AAA model and performed global proteomic and acetylomic analyses, identifying 7858 quantifiable proteins and 1790 acetylated proteins with 4581 acetylation sites. Bioinformatics analyses revealed that histones were enriched in pathways co-regulated by the proteome and acetylome and were modulated by histone acetyltransferases and deacetylases. Sirt2 and Sirt5 were predicted to inhibit neutrophil extracellular trap (NET) formation by suppressing histone acetylation, thereby potentially attenuating the progression of AAA. This study proposes that Sirt2 and Sirt5 may inhibit neutrophil extracellular trap (NET) formation by suppressing histone acetylation, potentially slowing AAA progression. Sirt2 and Sirt5 may represent potential therapeutic targets, providing a foundation for exploring the effect of the sirtuin protein family on AAA treatment.

Identifiers

PMID41322586
PMCPMC12658638

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.