Evidence mapPaperPMID 37709197Full record

ArticleJournal of advanced research2024

Evolocumab prevents atrial fibrillation in rheumatoid arthritis rats through restraint of PCSK9 induced atrial remodeling.

Xuejie Han, Yunlong Gao, Meijiao He, Yingchun Luo, Ying Wei, Yu Duan, Song Zhang, Hui Yu, Jiuxu Kan, Te Hou and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% of its field
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

Xuejie HanDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Yunlong GaoDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Meijiao HeDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Yingchun LuoDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Ying WeiDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Yu DuanDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Song ZhangDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Hui YuDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Jiuxu KanDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Te HouDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China.
Yun ZhangDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China. Electronic address: 263727@163.com.
Yue LiDepartment of Cardiology, the First Affiliated Hospital, Harbin Medical University, Harbin 150001, China; NHC Key Laboratory of Cell Translation, Harbin Medical University, Heilongjiang 150001, China; Key Laboratory of Hepatosplenic Surgery, Harbin Medical University, Ministry of Education, Harbin 150001, China; Key Laboratory of Cardiac Diseases and Heart Failure, Harbin Medical University, Harbin 150001, China; Heilongjiang Key Laboratory for Metabolic Disorder & Cancer Related Cardiovascular Diseases, Harbin 150081, China; Institute of Metabolic Disease, Heilongjiang Academy of Medical Science, Harbin, China. Electronic address: ly99ly@hrbmu.edu.cn.
Harbin Medical University · CNFirst Affiliated Hospital of Harbin Medical University · CNHeilongjiang Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionProprotein convertase subtilisin/kexin type 9 (PCSK9) is implicated in the pathogenesis and progression of autoimmune disease. Patients with rheumatoid arthritis (RA) are at high risk of developing atrial fibrillation (AF), while whether PCSK9 is involved in the onset of AF among RA patients remains unclear.

objectivesTo explore the role of PCSK9 in the occurrence of AF in RA patients and decipher the underlying mechanism.

methodsWe established a rat model of collagen-induced arthritis (CIA) by immunization with type II collagen in Freund's incomplete adjuvant. Atrial electrophysiological test was used to evaluate AF susceptibility. We performed a clinical study to examine the correlation between PCSK9 level and AF, which recruited healthy control, RA patients and RA patients complicated with AF. Evolocumab (a monoclonal antibody of PCSK9) is administered via intraperitoneal injection in CIA rats to assess the role of PCSK9 in RA-related AF. LPS-RS (LPS inhibitor), clodronate liposomes (depletion of macrophages), and cell co-culture model were used to dissect the mechanism underlying PCSK9 promotes AF.

resultsAF inducibility and duration were higher in CIA rats, accompanied by elevated plasma and atrial PCSK9. Interestingly, compared with healthy control subjects, patients with RA showed an increase in PCSK9, and the PCSK9 is much higher in RA patients complicated with AF. The level of PCSK9 was independently associated with AF risk in RA patients. In the in vivo experiment, evolocumab reduced AF susceptibility, and ameliorated atrial structural remodeling of CIA rats. Mechanistically, augmented LPS in CIA rats led to an increase in PCSK9, which exacerbated fibrosis of cardiac fibroblasts and apoptosis of cardiac myocytes by enhancement of M1 macrophages polarization and inflammation, thereby contributing to AF.

conclusionThis study suggests that elevated PCSK9 causes atrial structural remodeling by enhancement of M1 macrophages polarization in atria, and evolocumab can effectively protects CIA rats from AF.

Indexed as

Antibodies, Monoclonal, HumanizedArthritis, RheumatoidAtrial FibrillationAtrial RemodelingProprotein Convertase 9AnimalsArthritis, ExperimentalDisease Models, AnimalFemaleHeart AtriaHumansMacrophagesMaleMiddle AgedPCSK9 InhibitorsRatsAntibodies, Monoclonal, HumanizedevolocumabPCSK9 InhibitorsPCSK9 protein, humanPCSK9 protein, ratProprotein Convertase 9Atrial fibrillationEvolocumabPCSK9Rheumatoid arthritis

Identifiers

PMID37709197
PMCPMC11258665
OpenAlexW4386630416

What Socratic holds

Textmetadata
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.