Evidence map›Paper›PMID 40011664›Full record

ArticleScientific reports2025

PCSK9 with a gain of function D374Y mutation aggravates atherosclerosis by inhibiting PPARα expression.

Yuan Feng Cui, Xiao Cui Chen, Tuoluonayi Mijiti, Abidan Abudurusuli, Li Hui Deng, Xiang Ma, Bangdang Chen

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. Identification of a peptide inhibitor disrupting the PCSK9-LDLR interactionJournal of enzyme inhibition and medicinal chemistry · 2026
    Article
  2. Article
  3. Review
  4. Identification of Myeloid Protein Kinase C Epsilon as a Novel Atheroprotective Gene.Arteriosclerosis, thrombosis, and vascular biology · 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

7 authors.

Yuan Feng Cui *Xinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Xiao Cui Chen *Xinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Tuoluonayi MijitiXinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Abidan AbudurusuliXinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Li Hui DengXinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Xiang MaXinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Bangdang ChenXinjiang Key Laboratory of Cardiovascular Disease Research, State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, Clinical Medicine Institute, First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830011, Xinjiang, China. 6357@xjmu.edu.cn.

Funding

National Natural Science Foundation of China U1903304, 82160169, 82460175the Key Program of Natural Science Foundation of Xinjiang Uygur Autonomous Region 2022D01D16Tianshan Innovative Research Team Plan 2024D14011Xinjiang Uygur Autonomous Region Tianshan Youth Science and Technology Elite Talent Project 2022TSYCCX0031, 2023TSYCQNTJ0027
6 · The paper itself

Abstract

The preprotein convertase, Bacillus subtilis protease/kexin type 9 serine protease (PCSK9), has garnered significant attention as a potential lipid lowering and therapeutic drug target for atherosclerosis (AS). Peroxisome proliferator-activated receptor alpha (PPARα) is expressed in various tissues and has crucial roles in lipid metabolism and the inflammatory response; however, the precise impact of PCSK9 on AS progression through its regulation of PPARα remains uncertain. The present study aimed to examine the impact of introducing stable liver transduction of human derived PCSK9 with a gain of function D374Y mutation (PCSK9

Indexed as

AtherosclerosisGain of Function MutationPPAR alphaProprotein Convertase 9AnimalsDisease Models, AnimalHumansLipidsMacrophages, PeritonealMaleMiceMice, Inbred C57BLMice, KnockoutPlaque, AtheroscleroticLipidsPCSK9 protein, humanPcsk9 protein, mousePPAR alphaPpara protein, mouseProprotein Convertase 9AtherosclerosisInflammationLipoproteinsPeroxisome proliferator activated receptor alphaProprotein convertase subtilisin/Kexin type 9 Serine protease

Identifiers

PMID40011664
PMCPMC11865302

What Socratic holds

Texttitle and abstract
LicenceCC BY-NC-ND
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.