Evidence map›Paper›PMID 39587975›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Mechanical Activation of cPLA2 Impedes Fatty Acid β-Oxidation in Vein Grafts.

Linwei Fan, Yuanjun Tang, Jian Liu, Yueqi Liu, Yiwei Xu, Jiayu Liu, Han Liu, Wei Pang, Yuxuan Guo, Weijuan Yao and 3 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Mechanical Activation of cPLA2 Impedes Fatty Acid β-Oxidation in Vein Grafts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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

13 authors.

Linwei FanDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Yuanjun TangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Jian LiuShenzhen Bay Laboratory, Shenzhen, 518132, China.
Yueqi LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Yiwei XuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Jiayu LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Han LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Wei PangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Yuxuan GuoInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Weijuan YaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.
Tao ZhangDepartment of Vascular Surgery, Peking University People's Hospital, Beijing, 100044, China.
Qin PengShenzhen Bay Laboratory, Shenzhen, 518132, China.ORCID https://orcid.org/0000-0001-8364-3885
Jing ZhouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, National Health Commission Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University, Beijing, 100191, China.ORCID https://orcid.org/0000-0002-2211-4901

Funding

Guang-dong Pearl River Talent Program 2021QN02Y781Key Technologies Research and Development Program 2022YFC2704303National Natural Science Foundation of China 32100450National Natural Science Foundation of China 32171143National Natural Science Foundation of China 32325030National Natural Science Foundation of China 81921001National Natural Science Foundation of China 81970409National Natural Science Foundation of China 82270419Noncommunicable Chronic Diseases-National Science and Technology Major Project 2023ZD0503100Outstanding Youth Research Fund of Peking University People's Hospital RZ2022-05Research Project of Peking University Third Hospital in State Key Laboratory of Vascular Homeostasis and RemodelingShenzhen Bay Scholars ProgramShenzhen Medical Research Fund B2402010Special Project of Beijing-Tianjin-Hebei Basic Research Cooperation of Beijing Natural Science Foundation J230027
6 · The paper itself

Abstract

High-magnitude cyclic stretch from arterial blood pressure significantly contributes to the excessive proliferation and migration of vascular smooth muscle cells (VSMCs), leading to neointima formation in vein grafts. However, the molecular mechanisms remain unclear. This study highlights the critical role of cytosolic Phospholipase A2 (cPLA2)/ Yin Yang 1 (YY1)/ carnitine palmitoyltransferase 1b (CPT1B) signaling in coordinating VSMC mechanical activation by inhibiting fatty acid β-oxidation. Metabolomic analysis showed that a 15%-1 Hz arterial cyclic stretch, compared to a 5%-1 Hz venous stretch, increased long-chain fatty acids in VSMCs. cPLA2, identified as a mechanoresponsive molecule, produces excessive arachidonic acid (ArAc) under the 15%-1 Hz stretch, inhibiting CPT1B expression, a key enzyme in fatty acid β-oxidation. ArAc promotes transcription factor YY1 degradation, downregulating CPT1B. Inadequate fatty acid oxidation caused by knockdown of CPT1B or YY1, or etomoxir treatment, increased nuclear membrane tension, orchestrating the activation of cPLA2. Overexpressing CPT1B or inhibiting cPLA2 reduced VSMC proliferation and migration in vein grafts, decreasing neointimal hyperplasia. This study uncovers a novel mechanism in lipid metabolic reprogramming in vein grafts, suggesting a new therapeutic target for vein graft hyperplasia.

Indexed as

Fatty AcidsPhospholipases A2, CytosolicAnimalsCarnitine O-PalmitoyltransferaseCell ProliferationMaleMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleOxidation-ReductionCarnitine O-PalmitoyltransferaseFatty AcidsPhospholipases A2, Cytosoliccell proliferation and migrationfatty acid β‐oxidationmechanical forcemechanosensoryvascular smooth muscle cell

Identifiers

PMID39587975
PMCPMC11744522

What Socratic holds

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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.