Evidence map›Paper›PMID 41487086›Full record

ArticleCirculation2026

Histone Lactylation-Mediated Metabolic Remodeling in Vascular Smooth Muscle Cells Aggravates Aortic Aneurysm and Dissection by Promoting Lactate Accumulation.

Liwei Liu, Jinyan Zhang, Zhen Dong, Yikai Cui, Xiaoyi Zou, Hao Lai, Jiawei Gu, Xinyu Weng, Xuejuan Jin, Tianyi Qiu and 10 more

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In one paragraph

Article in Circulation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it

0cells of the map it votes in

15citing 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

15 citing papers in PubMed.

Identification of a Lactylation-Related Gene Signature and Candidate Biomarkers for Dilated Cardiomyopathy.Journal of cellular and molecular medicine · 2026
Article
Targeted Catalytic Anti-Inflammatory and Antioxidant Therapy for Aortic Dissection Using Biomimetic Nanomaterials.ACS omega · 2026
Article
Lactate as a Cardiovascular Exerkine: Mechanisms, Signaling Pathways, and Clinical Implications.Biomolecules · 2026
Review
Lactate Metabolism Dysregulation Drives the Pathogenesis of Acute Kidney Injury.Metabolites · 2026
Article
Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026
Review
Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026
Review
Targeting Endothelial PDK4-EndoMT Feedback Loop Mitigates the Development of Thoracic Aortic Dissection in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2026
Article
POU2F1 Promotes Chemoresistance in Colorectal Cancer Cells via Attenuates the MDR2 Degradation Mediated by PPP1R11 Lactylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
Article
PDK4 drives abdominal aortic aneurysm by promoting smooth muscle cell metabolic reprogramming and NLRP3-mediated pyroptosis.Nature communications · 2026
Article
Study on the Role and Mechanism ofJournal of cardiovascular development and disease · 2026
Article
Mitochondrial dysfunction in aortic aneurysm and dissection: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026
Review
Aortic dissection as a disease of vascular wall homeostasis: integrating vasa vasorum-inflammation-metabolism axis for mechanistic insight and clinical translation.Frontiers in immunology · 2026
Review
Lactate and lactylation in sepsis: regulation of immune-metabolic crosstalk and organ injury.Frontiers in immunology · 2026
Review
Trained Immunity-Like Memory in Vascular Structural Cells: Metabolic-Epigenetic Reprogramming as a Driving Mechanism of Atherosclerosis and Residual Cardiovascular Risk.Journal of inflammation research · 2026
Review
Lactylation Modification: From Basic Biological Process to Clinical Cardiovascular Diseases.Research (Washington, D.C.) · 2026
Review

4 · The record

Corrections and comments

Erratum issued
Correction to: Histone Lactylation-Mediated Metabolic Remodeling in Vascular Smooth Muscle Cells Aggravates Aortic Aneurysm and Dissection by Promoting Lactate Accumulation.2026

5 · Who and what money

Authors and funding

20 authors.

Liwei Liu *State Key Laboratory of Cardiology (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0001-7209-9212

Jinyan Zhang *Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).

Zhen Dong *Department of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0002-9786-3886

Yikai Cui *State Key Laboratory of Cardiology (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0002-3372-1352

Xiaoyi Zou *Reproductive Medicine Center (X.Z.), Zhongshan Hospital, Fudan University, Shanghai, China.

Hao LaiDepartment of Cardiac Surgery (H.L., J.G.), Zhongshan Hospital, Fudan University, Shanghai, China.

Jiawei GuDepartment of Cardiac Surgery (H.L., J.G.), Zhongshan Hospital, Fudan University, Shanghai, China.

Xinyu WengDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0002-7620-0813

Xuejuan JinDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).

Tianyi QiuInstitute of Clinical Science (T.Q.), Zhongshan Hospital, Fudan University, Shanghai, China.

Zhiqiang PeiDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).

Wenxuan HongDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).

Ya HuangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0002-5991-8698

Wei LuoDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0001-9416-9592

Lihong PanDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0002-1995-2373

Xiaolei SunDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0001-8690-8746

Beijian ZhangDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).

Adilan ShalamuDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0001-5211-9642

Aijun SunDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0003-1488-0937

Junbo GeDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, Shanghai, China (L.L., J.Z., Z.D., Y.C., X.W., X.J., Z.P., W.H., Y.H., W.L., L.P., X.S., B.Z., A.S., A.S., J.G.).ORCID 0000-0002-9360-7332

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVascular smooth muscle cells (VSMCs) undergo phenotypic changes during the development of aortic aneurysm and dissection (AAD). Metabolism shifts from oxidative phosphorylation to glycolysis. Recent studies suggest that epigenetics plays a crucial role in AAD.

methodsThe epigenetic regulation of histone lactylation was analyzed in the aorta of patients with aortic aneurysm and in a murine model of AAD. Histone lactylation was also studied in VSMCs treated with angiotensin II. The epigenetic pathway involving H4K16 lactylation (H4K16la) was explored in vitro and in vivo. To examine the role of H4K16la in AAD formation, mice lacking Pdk1 or Kat7 in VSMCs were created. Mice were treated with pharmacological inhibitors of Pdk1 or Kat7. The levels of blood lactate, aortic lactate, and aortic H4K16la were compared between patients with aortic aneurysm and controls.

resultsHistone lactylation (H4K16la) was increased in the aortic tissues of patients with AAD and mice. Enhanced histone lactylation was linked to increased pyruvate dehydrogenase kinase 1 (PDK1) transcription, which accelerated lactate production in VSMCs. A positive feedback loop was identified involving H4K16la, PDK1, and lactate; this pathway alters the metabolism and phenotype of VSMCs. KAT7 (lysine acetyltransferase 7) was found to be a histone lactyltransferase for histone lactylation in VSMCs. Genetic or pharmacological inhibition of PDK1 or KAT7 decreased AAD injury by disrupting the H4K16la/PDK1/lactate pathway. Patients with AAD have elevated lactate in blood and aortic tissues and elevated H4K16la in aortic tissues compared with control patients.

conclusionsHistone lactylation changes the metabolism and phenotype of VSMC in AAD. Inhibition of PDK1 or KAT7 may be a novel approach to treat or prevent AAD.

Indexed as

Aortic AneurysmAortic DissectionHistonesLactic AcidMuscle, Smooth, VascularMyocytes, Smooth MuscleAnimalsCells, CulturedDisease Models, AnimalEpigenesis, GeneticFemaleHistone AcetyltransferasesHumansMaleMiceMice, Inbred C57BLHistone AcetyltransferasesHistonesLactic AcidPDK1 protein, humanPdk1 protein, mousePyruvate Dehydrogenase Acetyl-Transferring Kinaseaortic aneurysmaortic dissectionKAT7 protein, humanlactatesPDK1 protein, human

Identifiers

PMID41487086

DOI10.1161/CIRCULATIONAHA.125.072576

PMCPMC12952488

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LicenceCC BY-NC-ND

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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 Socratic graph.