Evidence map›Paper›PMID 28000893›Full record

ArticleMolecular medicine reports2017

Hyperlipidemia-induced apoptosis of hippocampal neurons in apoE(-/-) mice may be associated with increased PCSK9 expression.

Xue-Shan Zhao, Qi Wu, Juan Peng, Li-Hong Pan, Zhong Ren, Hui-Ting Liu, Zhi-Sheng Jiang, Gui-Xue Wang, Zhi-Han Tang, Lu-Shan Liu

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 45 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

10 authors at 3 institutions in 1 country.

Xue-Shan ZhaoInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Qi WuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Juan PengInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Li-Hong PanInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Zhong RenInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Hui-Ting LiuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Zhi-Sheng JiangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Gui-Xue WangCollege of Bioengineering, Chongqing University, Chongqing 400030, P.R. China.
Zhi-Han TangInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Lu-Shan LiuInstitute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan University of South China, Hengyang, Hunan 421001, P.R. China.
Hunan University · CNUniversity of South China · CNChongqing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperlipidemia is a risk factor for Alzheimer's disease (AD) and other neurodegenerative diseases. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a lipid regulatory gene involved in cell apoptosis. However, the function and mechanism of PCSK9 in neuronal apoptosis following hyperlipidemia remains to be elucidated. The present study established a hyperlipidemic mouse model by feeding a high‑fat diet (HFD) to 6‑week‑old apoE(‑/‑) mice. Plasma lipid levels, hippocampal lipid accumulation, hippocampal histology, and hippocampal neuronal apoptosis were all monitored for changes. The expression levels of PCSK9, β‑secretase 1 (BACE1), B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein (Bax), and caspase‑3 in hippocampal CA3 and CA1 neurons were also measured. Results demonstrated that a HFD increased the lipid accumulation in the CA3 hippocampus and the levels of plasma lipids, including triglycerides, total cholesterol, low‑density lipoprotein, and high‑density lipoprotein. In addition, CA3 neurons in the HFD group indicated apparent injuries and increased neuronal apoptosis, which are associated with the expression of Bcl‑2, Bax, and caspase‑3. A HFD also increased the expression levels of PCSK9 and BACE1. BACE1 promotes cleavage of amyloid precursor proteins to generate β‑amyloid peptide (Aβ), which induces neuronal apoptosis. Protein levels of Aβ are associated with the observation of amyloid plaques in the hippocampus of the HFD group. The results suggest that hyperlipidemia regulates neuronal apoptosis by increasing PCSK9 and BACE1 expression. Overall, the current study may elucidate the role of lipid metabolism disorder in AD pathogenesis.

Indexed as

Gene Expression RegulationAmyloid Precursor Protein SecretasesAnimalsApolipoproteins EApoptosisbcl-2-Associated X ProteinCaspase 3CholesterolDiet, High-FatHippocampusHyperlipidemiasImmunohistochemistryMiceMice, KnockoutNeuronsProprotein Convertase 9Amyloid Precursor Protein SecretasesApolipoproteins Ebcl-2-Associated X ProteinCaspase 3CholesterolPcsk9 protein, mouseProprotein Convertase 9Proto-Oncogene Proteins c-bcl-2Triglycerides

Identifiers

PMID28000893
PMCPMC5364825
OpenAlexW2563745995

What OpenQuestion holds

Texttitle and abstract
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 OpenQuestion graph.