Evidence map›Paper›PMID 38129288›Full record

ArticleCell cycle (Georgetown, Tex.)2023

High-density lipoprotein protects vascular endothelial cells from indoxyl sulfate insults through its antioxidant ability.

Ching Chen, Chia-Chi Chang, I-Ta Lee, Chun-Yao Huang, Feng-Yen Lin, Shing-Jong Lin, Jaw-Wen Chen, Ting-Ting Chang

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024
    Review
  9. Review
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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

8 authors at 3 institutions in 1 country.

Ching ChenDepartment and Institute of Pharmacology, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Chia-Chi ChangDepartments of Internal Medicine, College of Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan.
I-Ta LeeSchool of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
Chun-Yao HuangDepartments of Internal Medicine, College of Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan.
Feng-Yen LinDepartments of Internal Medicine, College of Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan.
Shing-Jong LinDepartments of Internal Medicine, College of Medicine, School of Medicine, Taipei Medical University, Taipei, Taiwan.
Jaw-Wen ChenDepartment and Institute of Pharmacology, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Ting-Ting ChangDepartment and Institute of Pharmacology, School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.ORCID 0000-0003-4116-7029
National Yang Ming Chiao Tung University · TWTaipei Medical University Hospital · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) patients have a high risk of cardiovascular disease. Indoxyl sulfate (IS) is a uremic toxin that has been shown to inhibit nitric oxide production and cause cell senescence by inducing oxidative stress. High-density lipoprotein (HDL) has a protective effect on the cardiovascular system; however, its impacts on IS-damaged endothelial cells are still unknown. This study aimed to explore the effects of exogenous supplement of HDL on vascular endothelial cells in a uremia-mimic environment. Tube formation, migration, adhesion, and senescence assays were used to evaluate the cell function of human aortic endothelial cells (HAECs). Reactive oxygen species generation was measured by using Amplex red assay. L-NAME and MCI186 were used as a nitric oxide synthase inhibitor and a free radical scavenger, respectively. HDL exerted anti-inflammatory and antioxidant effects via HIF-1α/HO-1 activation and IL-1β/TNF-α/IL-6 inhibition in IS-stimulated HAECs. HDL improved angiogenesis ability through upregulating Akt/eNOS/VEGF/SDF-1 in IS-stimulated HAECs. HDL decreased endothelial adhesiveness via downregulating VCAM-1 and ICAM-1 in IS-stimulated HAECs. Furthermore, HDL reduced cellular senescence via upregulating SIRT1 and downregulating p53 in IS-stimulated HAECs. Importantly, the above beneficial effects of HDL were mainly due to its antioxidant ability. In conclusion, HDL exerted a comprehensive protective effect on vascular endothelial cells against damage from IS through its antioxidant ability. The results of this study might provide a theoretical basis for potential HDL supplementation in CKD patients with endothelial damage.

Indexed as

AntioxidantsRenal Insufficiency, ChronicEndothelial CellsHumansIndicanLipoproteins, HDLAntioxidantsIndicanLipoproteins, HDLhigh-density lipoproteinindoxyl sulfateVascular endothelial cell

Identifiers

PMID38129288
PMCPMC10802207
OpenAlexW4390079000

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.