Evidence map›Paper›PMID 41339842›Full record

ArticleLipids in health and disease2025

Arachidonic acid protects against diabetes-induced atrial fibrillation.

Hong Peng, Shuqi Xu, Yuying Liu, Jiali Yuan, Chengcheng Li, Yuxue Huang, Zheng Ran, Hua Xiao

Abstract read
In one paragraph

Article in Lipids in health and disease, 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

8 authors.

Hong Peng *Department of Cardiovascular Medicine, Cardiovascular Research Center, The First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Shuqi Xu *Department of Cardiovascular Medicine, The Affiliated Yongchuan Hospital of Chongqing Medical University, Chongqing, China.ORCID http://orcid.org/0000-0003-0094-2527
Yuying Liu *Department of Pharmacy, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jiali YuanDepartment of Cardiology, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Chengcheng LiDepartment of Cardiovascular Medicine, Cardiovascular Research Center, The First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Yuxue HuangDepartment of Cardiovascular Medicine, Cardiovascular Research Center, The First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Zheng RanDepartment of Pharmacy, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hua XiaoDepartment of Cardiovascular Medicine, Cardiovascular Research Center, The First Affiliated Hospital of Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing, 400016, China. xiaohua@hospital.cqmu.edu.cn.ORCID http://orcid.org/0000-0002-6116-627X

Funding

Chongqing Municipal Postdoctoral Science Special Foundation 2024CQBSHTB3039Innovation and Development Program of the Yongchuan District Science and Technology Bureau 2025yc-cxfz10074National Natural Science Foundation of China 82500395Talent Program of The Affiliated Yongchuan Hospital of Chongqing Medical University YJRC2024013Talent Program of The First Affiliated Hospital of Chongqing Medical University 2025QDPY-17
6 · The paper itself

Abstract

backgroundDiabetes mellitus (DM) significantly increases the risk of atrial fibrillation (AF), yet the underlying mechanisms remain poorly defined. Arachidonic acid (AA), a key omega-6 fatty acid involved in redox and inflammatory regulation, has been implicated in cardiovascular homeostasis, but its role in diabetes-related atrial remodeling and AF susceptibility is unclear.

methodsAA levels were measured in atrial tissues and serum from diabetic mice and AF patients. Diabetic mice were supplemented with AA, followed by structural, electrophysiological, and molecular analyses. Transcriptional regulation was assessed using Cut&Tag and dual-luciferase assays. To evaluate the γ-glutamylcysteine synthetase (γ-GCS)/γ-glutamylcysteine (γ-GC) pathway, mice were treated with the γ-GCS inhibitor L-Buthionine- (S, R)-sulfoximine (BSO) or supplemented with γ-GC.

resultsAA levels were significantly decreased in diabetic mice and AF patients and negatively correlated with atrial size. AA supplementation reduced atrial remodeling, oxidative stress, inflammation, and AF inducibility in diabetic mice, largely via activation of the Nrf2/γ-GCS pathway. BSO treatment reversed these benefits, while γ-GC supplementation mimicked the effects of AA.

conclusionThese results reveal a previously unrecognized protective role of AA against diabetes-induced atrial remodeling and AF, primarily mediated via redox modulation, and suggest AA as a promising therapeutic target in diabetic atrial cardiomyopathy.

Indexed as

Arachidonic AcidAtrial FibrillationDiabetes Mellitus, ExperimentalAnimalsAtrial RemodelingButhionine SulfoximineFemaleGlutamate-Cysteine LigaseHeart AtriaHumansMaleMiceMice, Inbred C57BLNF-E2-Related Factor 2Oxidative StressArachidonic AcidButhionine SulfoximineGlutamate-Cysteine LigaseNF-E2-Related Factor 2Arachidonic acid (AA)Atrial fibrillation (AF)Diabetes mellitus (DM)Metabolomic profilingOxidative stressRedox modulation

Identifiers

PMID41339842
PMCPMC12781673

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.