Evidence map›Paper›PMID 40320451›Full record

ArticleScientific reports2025

Unveiling the protective role of ESM1 in endothelial cell proliferation and lipid reprogramming.

Yukun Li, Anbo Gao, Wenchao Zhou, Xing Tang, Tian Zeng, Tingyu Fan, Weimin Jiang, Min Tang, Fan Ouyang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

9 authors.

Yukun Li *Department of Assisted Reproductive Centre, Zhuzhou Central Hospital, Xiangya Hospital Zhuzhou Central South University, Central South University, Zhuzhou, Hunan, China.
Anbo Gao *Department of Cardiology, Xiangya Hospital Zhuzhou, Zhuzhou Central Hospital, Central South University, Central South University, Zhuzhou, Hunan, China.
Wenchao ZhouDepartment of Assisted Reproductive Centre, Zhuzhou Central Hospital, Xiangya Hospital Zhuzhou Central South University, Central South University, Zhuzhou, Hunan, China.
Xing TangDepartment of Assisted Reproductive Centre, Zhuzhou Central Hospital, Xiangya Hospital Zhuzhou Central South University, Central South University, Zhuzhou, Hunan, China.
Tian ZengDepartment of Assisted Reproductive Centre, Zhuzhou Central Hospital, Xiangya Hospital Zhuzhou Central South University, Central South University, Zhuzhou, Hunan, China.
Tingyu FanDepartment of Assisted Reproductive Centre, Zhuzhou Central Hospital, Xiangya Hospital Zhuzhou Central South University, Central South University, Zhuzhou, Hunan, China.
Weimin JiangDepartment of Cardiology, Xiangya Hospital Zhuzhou, Zhuzhou Central Hospital, Central South University, Central South University, Zhuzhou, Hunan, China.
Min TangDepartment of Cardio-Thoracic Surgery, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Fan OuyangDepartment of Cardiology, Xiangya Hospital Zhuzhou, Zhuzhou Central Hospital, Central South University, Central South University, Zhuzhou, Hunan, China. 9304117@csu.edu.cn.

Funding

National Natural Science Foundation of China 82303246Natural Science Foundation of Hunan Province 2021JJ50070Natural Science Foundation of Hunan Province 2023JJ41066
6 · The paper itself

Abstract

Palmitic acid (PA), being the most prevalent free fatty acid in the human, holds significant implications as a risk factor for atherosclerosis (AS) due to its ability to induce physiological dysfunction in endothelial cells (ECs). Endothelial cell-specific molecule 1 (ESM1), has been identified as a marker for activated ECs. Nevertheless, the mechanisms underlying ESM1-induced endothelial cell proliferation remain elusive. The expression of ESM1, ANGPTL4 and autophagy related protein were confirmed by western blot. Proliferation ability was tested by MTT and EdU. Lipids level was confirmed by Oil red staining. Autophagic flux was confirmed by Monodansylcadaverine (MDC) staining and pCMV-mCherry-GFP-LC3B fluorescence staining assay. The mouse model of AS was used to observe the effect of PA on the ESM1-ANGPTL4-autophagy signaling axis. This study elucidates ESM1-ANGPTL4 axis in maintaining proliferation of ECs and lipid reprogramming. Furthermore, it has been observed that PA has the ability to stimulate EC to autonomously increase the expression of ESM1, which in turn can counteract the detrimental effects of PA on ECs. Conversely, when ESM1 is suppressed, the damaging effects of PA on ECs are exacerbated. Mechanistically, our findings indicate that ESM1 facilitates EC proliferation and lipids homeostasis by up-regulating autophagy through ANGPTL4. This effect of ESM1 on ECs can be attenuated by ATG7 inhibiting. Additionally, the serum levels of ESM1 were found to be elevated in AS mice. ESM1 was found to enhance ECs proliferation and mitigate endothelial cell injury induced by PA through the upregulation of autophagy. This mechanism potentially serves as a protective factor against atherosclerosis progression.

Indexed as

AtherosclerosisCell ProliferationEndothelial CellsLipid MetabolismProteoglycansAngiopoietin-Like Protein 4AnimalsAutophagyDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsMiceMice, Inbred C57BLNeoplasm ProteinsPalmitic AcidSignal TransductionAngiopoietin-Like Protein 4ESM1 protein, humanNeoplasm ProteinsPalmitic AcidProteoglycansANGPTL4AutophagyEndothelial cell injuryESM1Lipid metabolism reprogrammingPalmitic acid

Identifiers

PMID40320451
PMCPMC12050336

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.