Evidence map›Paper›PMID 24649090›Full record

ArticleBiomedical reports2014

The dual behavior of PCSK9 in the regulation of apoptosis is crucial in Alzheimer's disease progression (Review).

Qi Wu, Zhi-Han Tang, Juan Peng, Ling Liao, Li-Hong Pan, Chun-Yan Wu, Zhi-Sheng Jiang, Gui-Xue Wang, Lu-Shan Liu

Open access · bronzeAbstract read
In one paragraph

Article in Biomedical reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
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  10. Review
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  12. Oxidized LDLs as Signaling Molecules.Antioxidants (Basel, Switzerland) · 2021
    Review
  13. Article
  14. Article
  15. Review
  16. Article
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  18. Article
  19. Article
  20. Inhibiting PCSK9 - biology beyond LDL control.Nature reviews. Endocrinology · 2018
    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

9 authors at 1 institution in 1 country.

Qi WuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Zhi-Han TangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China ; Bioengineering College of Chongqing University, Chongqing 400044, P.R. China.
Juan PengInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Ling LiaoInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Li-Hong PanInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Chun-Yan WuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Zhi-Sheng JiangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
Gui-Xue WangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China ; Bioengineering College of Chongqing University, Chongqing 400044, P.R. China.
Lu-Shan LiuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang, Hunan 421001, P.R. China.
University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal apoptosis is crucial in neurodegenerative diseases. However, a lower apoptotic rate of nerve cells is detected in the brain compared to that in other organs in neurodegenerative patients or in animal models, suggesting that neuronal apoptosis induced by any type of risk factors is intricately regulated. Human and animal studies demonstrated that a high concentration of oxidized LDL (ox-LDL) in the brain, which is associated with hyperlipidemia, is one of the key apoptosis inducers in neurodegenerative diseases. However, the mechanism underlying the ox-LDL-mediated regulation of neuronal apoptosis has not been fully elucidated. Recently, we investigated proprotein convertase subtilisin/kexin type 9 (PCSK9), a striking gene involved in lipid metabolism that exhibits a positive correlation with macrophage and endothelial cell apoptosis induced by ox-LDL. Moreover, PCSK9 may degrade β-site amyloid precursor protein-cleaving enzyme 1 (BACE1), the key enzyme cleaving amyloid precursor protein (APP) to generate amyloid β peptide (Aβ). Aβ is another key apoptosis inducer in neurodegenerative diseases. Our findings indicated that PCSK9 may be upregulated by the high levels of ox-LDL in the brain associated with hyperlipidemia and promote neuronal apoptosis through the NF-κB-B-cell lymphoma 2 (Bcl-2)/Bax-caspase 9-caspase 3 signaling pathways. Moreover, increased PCSK9 levels may inhibit the APP/Aβ metabolic pathway and reduce Aβ generation by degrading BACE1, thereby decreasing Aβ-induced neuronal apoptosis. The dual regulation mechanism of PCSK9 on apoptosis maintains neuronal apoptosis induced by risk factors at low levels.

Indexed as

Alzheimer’s diseaseamyloid β peptideapoptosisoxidized low-density lipoproteinproprotein convertase subtilisin/kexin type 9β-site amyloid precursor protein-cleaving enzyme 1

Identifiers

PMID24649090
PMCPMC3917750
OpenAlexW2033141013

What OpenQuestion holds

Textmetadata
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.