Evidence map›Paper›PMID 40398746›Full record

ArticleJournal of advanced research2026

Ketogenic diet and β-hydroxybutyrate inhibit HDAC1 to preserve vascular smooth muscle cell function in thoracic aortic aneurysm.

Xinyu Weng, Lihong Pan, Xiurui Ma, Wei Luo, Hongdong Su, Zhiqiang Pei, Zhen Dong, Liwei Liu, Jing Yang, Pingjin Gao and 1 more

Registry-linked trialAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07495267 (Nutritional Ketosis as a Novel Therapeutic Strategy to Stabilize Chronic Aortic Dissection in Marfan Syndrome), which is not on this map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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.

NCT07495267 nanot yet recruitingnot on this map

Nutritional Ketosis as a Novel Therapeutic Strategy to Stabilize Chronic Aortic Dissection in Marfan Syndrome

TypeinterventionalSponsorWashington University School of MedicineRan2026 to 2028Enrolled15ConditionsMarfan Syndrome, Aortic DissectionArmsKetogenic diet
3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Review
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.

Xinyu WengDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Lihong PanDepartment of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA.
Xiurui MaDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Wei LuoCenter for Coronary Artery Disease, Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Hongdong SuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhiqiang PeiOriental Pan-Vascular Devices Innovation College, University of Shanghai for Science and Technology, Shanghai, China.
Zhen DongDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Liwei LiuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Jing YangDepartment of Cardiology, Shanghai Xuhui Central Hospital, Zhongshan-Xuhui Hospital, Fudan University, Shanghai, China. Electronic address: jing_yang@fudan.edu.cn.
Pingjin GaoDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Aijun SunDepartment of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China; State Key Laboratory of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China. Electronic address: sun.aijun@zs-hospital.sh.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThoracic aortic aneurysm (TAA) is a serious condition characterized by dilation of the thoracic aorta, often leading to aortic dissection or rupture. Current treatments involve surgical and pharmacological interventions and do not effectively address the underlying molecular mechanisms. This study explores the effects of ketogenic diet (KD) on TAA, focusing on histone deacetylase 1 (HDAC1) and vascular smooth muscle cells (VSMCs) function.

methodsA β-aminopropionitrile monofumarate (BAPN)-induced TAA mouse model was used. Mice were divided into groups receiving either a standard diet or KD. Additionally, β-hydroxybutyrate (BHB), a KD-derived ketone body, and parthenolide or ITSA-1 were administered. The study measured survival rates, aortic dilation, elastin degradation, VSMC contractile markers, mitochondrial function, and oxidative stress levels.

resultsKD significantly improved survival rates and reduced aortic dilation and elastin degradation in the TAA mouse model. BHB also mitigated TAA development, demonstrating similar protective effects. KD and BHB were particularly effective in preserving mitochondrial function and maintaining VSMC contractile phenotype by restoring contractile marker expression. Additionally, KD and BHB significantly reduced oxidative stress levels. The addition of HDAC1 inhibitor parthenolide or HDAC agonist ITSA-1 further evaluated the protective effects of BHB against vascular damage.

conclusionOur study reveals the important roles of KD and BHB in regulating HDAC1, preserving mitochondrial function, maintaining VSMC phenotype, and reducing oxidative stress in TAA. Our findings demonstrate KD and BHB as promising therapeutic strategies for treating TAA by targeting specific molecular pathways involved in its progression. This study highlights the significance and innovation of lifestyle interventions, such as KD, in mitigating TAA by addressing its underlying molecular mechanisms.

Indexed as

3-Hydroxybutyric AcidAortic Aneurysm, ThoracicDiet, KetogenicHistone Deacetylase 1Muscle, Smooth, VascularMyocytes, Smooth MuscleAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLOxidative Stress3-Hydroxybutyric AcidHdac1 protein, mouseHistone Deacetylase 1Histone deacetylase 1Ketogenic dietThoracic aortic aneurysmVascular Remodelingβ-hydroxybutyrate

Identifiers

PMID40398746
PMCPMC12869236

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Registered trials

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.