Evidence map›Paper›PMID 32021943›Full record

ArticleHeliyon2020

Autophagy activation is required for homocysteine-induced apoptosis in bovine aorta endothelial cells.

Keisuke Sato, Tomonari Nishii, Ayana Sato, Ryosuke Tatsunami

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
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

4 authors at 1 institution in 1 country.

Keisuke SatoDepartment of Pharmacy, Hokkaido University of Science, 7-15-4-1 Maeda, Teine, Sapporo, Hokkaido, 006-8585, Japan.
Tomonari NishiiDepartment of Pharmacy, Hokkaido University of Science, 7-15-4-1 Maeda, Teine, Sapporo, Hokkaido, 006-8585, Japan.
Ayana SatoDepartment of Pharmacy, Hokkaido University of Science, 7-15-4-1 Maeda, Teine, Sapporo, Hokkaido, 006-8585, Japan.
Ryosuke TatsunamiDepartment of Pharmacy, Hokkaido University of Science, 7-15-4-1 Maeda, Teine, Sapporo, Hokkaido, 006-8585, Japan.
Hokkaido University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An elevated level of homocysteine (Hcy) in plasma is an independent risk factor for cardiovascular disease and central nervous system disease. Endothelial dysfunction as a result of apoptosis in endothelial cells is involved in the development and progression of these diseases. In this study, we aimed to investigate the effect of autophagy activation by amino acid starvation on Hcy-induced cytotoxicity in bovine aorta endothelial cells (BAECs). Hcy-induced lactate dehydrogenase (LDH) release was promoted by amino acid starvation. In addition, Hcy increased cleaved caspase-3 level, an indicator of apoptosis, by amino acid starvation. We revealed that oxidative stress is not involved in the Hcy-induced cytotoxicity promoted by amino acid starvation. Salazosulfapyridine (SASP), an SLC7A11 inhibitor, protected against the Hcy-induced LDH release promoted by amino acid starvation. SASP decreased the Hcy-induced cleaved caspase-3 level by amino acid starvation. We demonstrate for the first time that autophagy activation by amino acid starvation promotes Hcy-induced apoptosis in BAECs. Moreover, SLC7A11 inhibitor SASP, which is an amino acid transporter, protects against Hcy-induced apoptosis due to autophagy.

Indexed as

AntioxidantApoptosisAutophagyBiochemistryBiological sciencesBovine aorta endothelial cellCell biologyCell deathCytotoxicityHomocysteineOxidative stressSLC7A11Toxicology

Identifiers

PMID32021943
PMCPMC6994847
OpenAlexW3003436676

What OpenQuestion holds

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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.