Evidence map›Paper›PMID 32169071›Full record

ReviewCardiovascular diabetology2020

Research progress on alternative non-classical mechanisms of PCSK9 in atherosclerosis in patients with and without diabetes.

Ying Tang, Sheng-Lan Li, Jia-Hui Hu, Kai-Jun Sun, Lei-Ling Liu, Dan-Yan Xu

Open access · goldFull text readReview
In one paragraph

Review in Cardiovascular diabetology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

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  18. Lipid oxidation in pathophysiology of atherosclerosis: Current understanding and therapeutic strategies.International journal of cardiology. Cardiovascular risk and prevention · 2022
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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

6 authors at 2 institutions in 1 country.

Ying TangDepartment of Internal Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China.
Sheng-Lan LiDepartment of Internal Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China.
Jia-Hui HuDepartment of Internal Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China.
Kai-Jun SunDepartment of Internal Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China.
Lei-Ling LiuDepartment of Internal Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China.
Dan-Yan XuDepartment of Internal Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, 139 Middle Renmin Road, Changsha, 410011, Hunan, China. xudanyan02@csu.edu.cn.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The proprotein convertase subtilisin/kexin type 9 (PCSK9) acts via a canonical pathway to regulate circulating low-density lipoprotein-cholesterol (LDL-C) via degradation of the LDL receptor (LDLR) on the liver cell surface. Published research has shown that PCSK9 is involved in atherosclerosis via a variety of non-classical mechanisms that involve lysosomal, inflammatory, apoptotic, mitochondrial, and immune pathways. In this review paper, we summarized these additional mechanisms and described how anti-PCSK9 therapy exerts effects through these mechanisms. These additional pathways further illustrate the regulatory role of PCSK9 in atherosclerosis and offer an in-depth interpretation of how the PCSK9 inhibitor exerts effects on the treatment of atherosclerosis.

Indexed as

AnimalsAntibodies, MonoclonalAnticholesteremic AgentsAtherosclerosisCholesterol, LDLDiabetes MellitusDyslipidemiasEndothelial CellsHumansInflammationMacrophagesPCSK9 InhibitorsPlaque, AtheroscleroticProprotein Convertase 9Serine Proteinase InhibitorsAntibodies, MonoclonalAnticholesteremic AgentsCholesterol, LDLPCSK9 InhibitorsPCSK9 protein, humanProprotein Convertase 9Serine Proteinase InhibitorsAtherosclerosisInflammationLDL-CMitochondrial DNAPCSK9

Identifiers

PMID32169071
PMCPMC7071562
OpenAlexW3011320855

What Socratic holds

Textfull text, public
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.