Evidence map›Paper›PMID 39424784›Full record

ArticleCell death & disease2024

Latexin deficiency limits foam cell formation and ameliorates atherosclerosis by promoting macrophage phenotype differentiation.

Guozhang He, Yuanting Ni, Rong Hua, Huaibin Wan, Yanhui Tan, Qiwei Chen, Shaohua Xu, Yuzhong Yang, Lijun Zhang, Wei Shu and 4 more

Abstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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

8 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Targeted drug delivery systems for atherosclerosis.Journal of nanobiotechnology · 2025
    Review
  7. Article
  8. 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

14 authors.

Guozhang He *State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China.
Yuanting Ni *State Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China.
Rong Hua *Department of Scientific Research, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Huaibin Wan *Heyuan Research Center for Cardiovascular Diseases, Department of Cardiology, the Fifth Affiliated Hospital of Jinan University, Heyuan, Guangdong, China.
Yanhui TanState Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China.
Qiwei ChenDepartment of Scientific Research, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
Shaohua XuState Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China.
Yuzhong YangDepartment of Pathology, Affiliated Hospital of Guilin Medical College, Guilin, China.
Lijun ZhangState Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China.
Wei ShuCollege of Intelligent Medicine and Biotechnology, Guilin Medical University, Guilin, China.
Ke-Bin HuangState Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China.
Yi MoBiobank department, The reproductive hospital of Guangxi Zhuang autonomous region, Nanning, China.
Hong LiangState Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China. hliang@gxnu.edu.cn.
Ming ChenState Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources, Key Laboratory for Chemistry and Molecular Engineering of Medicinal Resources (Ministry of Education of China), School of Chemistry and Pharmaceutical Sciences, Guangxi Normal University, Guilin, China. chenmingprotein@mailbox.gxnu.edu.cn.ORCID 0000-0001-5935-7694

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82360098
6 · The paper itself

Abstract

Latexin (LXN) is abundant in macrophages and plays critical roles in inflammation. Much is known about macrophages in atherosclerosis, the role of macrophage LXN in atherosclerosis has remained elusive. Here, the expression of LXN in human and mouse atherosclerotic lesions was examined by immunofluorescence and immunohistochemistry. LXN knockout and LXN/ApoE double-knockout mice were generated to evaluate the functions of LXN in atherosclerosis. Bone marrow transplantation (BMT) experimentation was carried out to determine whether macrophage LXN regulates atherosclerosis. We found that LXN is enriched in human and murine atherosclerotic lesions, mainly localized to macrophages. LXN deletion ameliorated atherosclerosis in ApoE

Indexed as

AtherosclerosisFoam CellsMacrophagesPhenotypeAnimalsApolipoproteins ECell DifferentiationHumansMaleMiceMice, Inbred C57BLMice, KnockoutSTAT3 Transcription FactorApolipoproteins ESTAT3 Transcription Factor

Identifiers

PMID39424784
PMCPMC11492231

What OpenQuestion 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 OpenQuestion graph.