Evidence mapPaperPMID 42375844Full record

ArticleFrontiers in cardiovascular medicine2026

PCSK9 promotes atherosclerosis progression through the FOXO3a autophagy signaling pathway.

Yuanjia Shi, Jing Zhang, Lina Dai, Jie Chen, Shijia Geng, Yan Niu, Chongyang Dong, Chenlei Li, Rujin Liu, Ningxia Zhao and 4 more

Abstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Yuanjia Shi *Department of Basic Medicine, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, China.
Jing Zhang *Department of Basic Medicine, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, China.
Lina Dai *College of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Jie ChenCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Shijia GengCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Yan NiuMedical Experiments Center, Inner Mongolia Medical University, Hohhot, China.
Chongyang DongCollege of Traditional Chinese Medicine, Inner Mongolia Medical University, Hohhot, China.
Chenlei LiDepartment of Basic Medicine, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, China.
Rujin LiuDepartment of Basic Medicine, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, China.
Ningxia ZhaoDepartment of Basic Medicine, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, China.
Xiaomeng WangDepartment of Basic Medicine, School of Basic Medical Sciences, Inner Mongolia Medical University, Hohhot, China.
Zhanfeng GaoDepartment of Cardiology, The Affiliated Hospital, Inner Mongolia Medical University, Hohhot, China.
Xi YangCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.
Shang GaoCollege of Basic Medicine, Inner Mongolia Medical University, Hohhot, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: The proprotein convertase subtilisin/kexin type 9 (PCSK9) has an impact on atherosclerosis by modulating the autophagy pathway; however, its precise mechanisms underlying autophagy require additional investigation. Methodology and results: ApoE-/- male mice were fed high-fat diets, different doses of COS (Chitosan oligosaccharide) or JY2 were given by gavage, and RAPA or CQ was injected intraperitoneally. The immunofluorescence intensities of PCSK9, FOXO3a and LC3, collagen fibers and calcium salt deposition in aortic sinus tissues were measured. Conclusions and significance: PCSK9 promotes macrophage autophagy injury and facilitates atherosclerosis progression through activation of the FOXO3a autophagy pathway, whereas COS reduces PCSK9 injury to macrophages and atherosclerosis. These findings provide a theoretical basis and experimental foundation for the future development of PCSK9 inhibitors as a new strategy for the treatment of As.

Indexed as

atherosclerosisautophagyCOSFOXO3aPCSK9

Identifiers

PMID42375844
PMCPMC13310736

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.