Evidence map›Paper›PMID 41918565›Full record

ReviewFrontiers in cardiovascular medicine2026

LDL receptor-independent mechanisms of proprotein convertase subtilisin/kexin type 9 in cardiovascular pathophysiology.

Hang Su, Xunan Guo, Qiang Li, Xiaohang Yuan, Xiaolong Wu, Zihan Zhao, Yi Kan, Yifan Yang, Zhaolin Fu, Zhenrui Qi and 1 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Hang SuInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Xunan GuoInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Qiang LiInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Xiaohang YuanInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Xiaolong WuInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Zihan ZhaoInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yi KanInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yifan YangInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Zhaolin FuInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Zhenrui QiInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Guangyuan SongInterventional Center of Valvular Heart Disease, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a pivotal regulator of lipid metabolism and a validated therapeutic target in cardiovascular disease (CVD). While its canonical role in mediating low-density lipoprotein receptor (LDLR) degradation underpins its cholesterol-lowering effects, emerging evidence highlights diverse LDLR-independent actions that contribute to cardiovascular pathology. PCSK9 exerts pro-inflammatory, pro-atherosclerotic, pro-thrombotic, and cardiotoxic effects and promotes valvular calcification-thereby influencing vascular, myocardial, and structural heart disease beyond lipid regulation. This review delineates these non-canonical mechanisms, emphasizing PCSK9's roles in vascular inflammation, atherosclerosis, thrombosis, regulated cardiomyocyte death, and calcific aortic valve disease (CAVD). We also address key unresolved questions regarding the "efficacy gap" between pharmacological inhibition and lifelong genetic deficiency and examine the translational implications for next-generation inhibitors, including small molecules, vaccines, and gene-editing therapies. A deeper understanding of PCSK9's pleiotropic functions may inform precision strategies to achieve cardiovascular protection extending beyond LDL-C lowering.

Indexed as

calcific aortic valve disease (CAVD)cardiomyocyte deathcardiovascular disease (CVD)efficacy gapinflammationlow-density lipoprotein receptor (LDLR)proprotein convertase subtilisin/kexin type 9 (PCSK9)thrombosis

Identifiers

PMID41918565
PMCPMC13033574

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.