Evidence map›Paper›PMID 39853712›Full record

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

ACSL1 Aggravates Thromboinflammation by LPC/LPA Metabolic Axis in Hyperlipidemia Associated Myocardial Ischemia-Reperfusion Injury.

Shuai Jiang, Xueguang Lin, Bo Chen, Gang Chen, Kristine J S Kwan, Jing Liu, Qi Sun, Jie Wang, Yijie Lu, Jindong Tong 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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Catalpol-a compound fromFrontiers in microbiology · 2025
    Article
  13. 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.

Shuai JiangShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.ORCID https://orcid.org/0000-0002-4203-5557
Xueguang LinShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Bo ChenShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Gang ChenDepartment of Cardiology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Kristine J S KwanShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Jing LiuState Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, and Human Phenome Institute, Fudan University, Shanghai, 200438, China.
Qi SunDepartment of Endocrinology and Metabolism, Affiliated Hospital of Nantong University, Nantong, 226006, China.
Jie WangShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Yijie LuShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Jindong TongShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Ying DengShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Bo YuShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.
Jingdong TangShanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai, 201399, China.ORCID https://orcid.org/0009-0006-4849-9973

Funding

Health and Family Planning Committee of Pudong New Area PKJ2023-Y04Health and Family Planning Committee of Pudong New Area PWRq2023-19Shanghai Pudong New Area Health Commission PWZxk2022-01
6 · The paper itself

Abstract

Acute myocardial infarction (AMI) is associated with well-established metabolic risk factors, especially hyperlipidemia and obesity. Myocardial ischemia-reperfusion injury (mIRI) significantly offsets the therapeutic efficacy of revascularization. Previous studies indicated that disrupted lipid homeostasis can lead to lipid peroxidation damage and inflammation, yet the underlying mechanisms remain unclear. Here, the study demonstrates that hyperlipidemia is a key driver of mIRI. Long-chain fatty acyl-CoA synthetase 1 (ACSL1) is upregulated in both hyperlipidemia and AMI patients. ACSL1 expression is induced by a high-fat microenvironment (oxLDL and palmitic acid) in a concentration-dependent manner. Interestingly, the protein level is positively correlated with total cholesterol level and thromboinflammatory biomarkers. Furthermore, ACSL1 reprogrammed lipid metabolism in monocytes, leading to the accumulation of lysophosphatidylcholine (LPC)/lysophosphatidic acid (LPA). The monocytic LPC/LPA axis accelerated lipid peroxidation and neutrophil extracellular traps (NETs)-induced thromboinflammation via the paracrine effect. The main LPA producer Autotaxinis is also induced under high-fat conditions and then exerts thromboinflammation response through converted LPC to LPA. Finally, ACSL1 knockdown or NETs release inhibitor (DNase I or GSK484) significantly alleviated mIRI in mice. These findings highlight ACSL1 and NETosis as potential key targets for preventing mIRI and underscore the lipid peroxidation in the mechanisms of ACSL1-mediated thromboinflammation.

Indexed as

Coenzyme A LigasesHyperlipidemiasInflammationLysophosphatidylcholinesLysophospholipidsMyocardial Reperfusion InjuryThrombosisAnimalsHumansLipid MetabolismMaleMiceMice, Inbred C57BLMyocardial InfarctionACSL1 protein, humanCoenzyme A Ligaseslysophosphatidic acidLysophosphatidylcholinesLysophospholipidsACSL1hyperlipidemiaischemia‐reperfusion injurylipid metabolismthromboinflammation

Identifiers

PMID39853712
PMCPMC11923997

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.