Evidence map›Paper›PMID 32725144›Full record

ArticleBioscience reports2020

KAP1 silencing relieves OxLDL-induced vascular endothelial dysfunction by down-regulating LOX-1.

Tianqing Yan, Chang Liang, Haidi Fan, Wei Zhou, Linyan Huang, Suhua Qi, Wan Wang, Ping Ma

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

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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

8 authors at 1 institution in 1 country.

Tianqing Yan *School of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Chang Liang *School of Basic Medical Science, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Haidi FanSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Wei ZhouSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Linyan HuangSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Suhua QiSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Wan WangSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Ping MaSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City 221004, Jiangsu Province, China.
Xuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KRAB domain-associated protein 1 (KAP1) is highly expressed in atherosclerotic plaques. Here, we studied the role of KAP1 in atherosclerosis development using a cell model of endothelial dysfunction induced by oxidative low-density lipoprotein (OxLDL). The phosphorylation and protein levels of KAP1 were similar between OxLDL-treated and non-treated endothelial cells (ECs). KAP1 depletion significantly inhibited the production of OxLDL-enhanced reactive oxygen species and the expression of adhesion molecules in ECs. Treatment with OxLDL promoted the proliferation and migration of ECs, which was also confirmed by the elevated levels of the proliferative markers c-Myc and PCNA, as well as the migratory marker MMP-9. However, these effects were also abrogated by KAP1 depletion. Moreover, the depletion of KAP1 in OxLDL-treated ECs resulted in decreases in the LOX-1 level and increases in eNOS expression. Generally, the data suggest that strategies targeting KAP1 depletion might be particularly useful for the prevention or treatment of atherosclerosis.

Indexed as

Gene SilencingCell LineCell MovementCell ProliferationDown-RegulationEndothelial CellsHumansLipoproteins, LDLNitric Oxide Synthase Type IIIPhosphorylationReactive Oxygen SpeciesScavenger Receptors, Class ESignal TransductionTripartite Motif-Containing Protein 28Lipoproteins, LDLNitric Oxide Synthase Type IIINOS3 protein, humanOLR1 protein, humanoxidized low density lipoproteinReactive Oxygen SpeciesScavenger Receptors, Class ETRIM28 protein, humanTripartite Motif-Containing Protein 28Endothelial dysfunction (ED)Endothelial nitric oxide synthase (eNOS)KRAB domain-associated protein 1 (KAP1)Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1)Oxidized low-density lipoprotein (OxLDL)

Identifiers

PMID32725144
PMCPMC7414520
OpenAlexW3045775172

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.