Evidence map›Paper›PMID 34782856›Full record

ReviewFrontiers in cardiovascular medicine2021

Regulation of PCSK9 Expression and Function: Mechanisms and Therapeutic Implications.

Xiao-Dan Xia, Zhong-Sheng Peng, Hong-Mei Gu, Maggie Wang, Gui-Qing Wang, Da-Wei Zhang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
13.4field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. PCSK9 in critical illness - It's not all about lipids.Annals of clinical biochemistry · 2026
    Review
  8. PCSK9 orchestrates the antigen presentation-endothelial barrier axis to potentiate immune exclusion in colorectal cancer.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  9. Review
  10. Review
  11. Enzyme-Assisted Synthesis and In Vitro Characterization of Bifunctional PCSK9 Inhibitors.Chembiochem : a European journal of chemical biology · 2026
    Article
  12. Article
  13. Article
  14. Diallyl trisulfide attenuates metabolic syndromeFrontiers in pharmacology · 2026
    Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review
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

6 authors at 3 institutions in 2 countries.

Xiao-Dan XiaDepartment of Orthopedics, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, China.
Zhong-Sheng PengSchool of Economics, Management and Law, University of South China, Hengyang, China.
Hong-Mei GuGroup on the Molecular and Cell Biology of Lipids, Department of Pediatrics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada.
Maggie WangGroup on the Molecular and Cell Biology of Lipids, Department of Pediatrics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada.
Gui-Qing WangDepartment of Orthopedics, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, China.
Da-Wei ZhangGroup on the Molecular and Cell Biology of Lipids, Department of Pediatrics, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada.
University of Alberta · CAGuangzhou Medical University · CNUniversity of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) promotes degradation of low-density lipoprotein receptor (LDLR) and plays a central role in regulating plasma levels of LDL cholesterol levels, lipoprotein(a) and triglyceride-rich lipoproteins, increasing the risk of cardiovascular disease. Additionally, PCSK9 promotes degradation of major histocompatibility protein class I and reduces intratumoral infiltration of cytotoxic T cells. Inhibition of PCSK9 increases expression of LDLR, thereby reducing plasma levels of lipoproteins and the risk of cardiovascular disease. PCSK9 inhibition also increases cell surface levels of major histocompatibility protein class I in cancer cells and suppresses tumor growth. Therefore, PCSK9 plays a vital role in the pathogenesis of cardiovascular disease and cancer, the top two causes of morbidity and mortality worldwide. Monoclonal anti-PCSK9 antibody-based therapy is currently the only available treatment that can effectively reduce plasma LDL-C levels and suppress tumor growth. However, high expenses limit their widespread use. PCSK9 promotes lysosomal degradation of its substrates, but the detailed molecular mechanism by which PCSK9 promotes degradation of its substrates is not completely understood, impeding the development of more cost-effective alternative strategies to inhibit PCSK9. Here, we review our current understanding of PCSK9 and focus on the regulation of its expression and functions.

Indexed as

atherosclerosiscancer immunotherapycardiovascular diseaseLDL receptorlipid metabolismmajor histocompatibility protein class IPCSK9

Identifiers

PMID34782856
PMCPMC8589637
OpenAlexW3208891341

What OpenQuestion 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 OpenQuestion graph.