Evidence map›Paper›PMID 25013404›Full record

ArticleJournal of biomedical research2014

Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage.

Hanpeng Huang, Xiaoyu Li, Yan Zhuang, Nan Li, Xudong Zhu, Jin Hu, Jingjing Ben, Qing Yang, Hui Bai, Qi Chen

Open access · hybridAbstract read
In one paragraph

Article in Journal of biomedical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  4. The Role of Hydrogen Sulfide Regulation of Autophagy in Liver Disorders.International journal of molecular sciences · 2022
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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 1 institution in 1 country.

Hanpeng HuangAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China;
Xiaoyu LiAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China; ; State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Yan ZhuangState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Nan LiAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China;
Xudong ZhuState Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Jin HuAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China;
Jingjing BenAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China;
Qing YangAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China;
Hui BaiAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China;
Qi ChenAtherosclerosis Research Centre, Laboratory of Molecular Intervention for Cardiovascular Diseases, Nanjing Medical University, Nanjing, Jiangsu 210029, China; ; State Key Laboratory of Reproductive Medicine, Nanjing Medical University, Nanjing, Jiangsu 210029, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage death in advanced atherosclerosis promotes plaque necrosis and destabilization. Involvement of autophagy in bulk degradation of cellular components has been recognized recently as an important mechanism for cell survival under endoplasmic reticulum (ER) stress. We previously found that the engagement of class A scavenger receptor (SR-A) triggered JNK-dependent apoptosis in ER-stressed macrophages. However, pro-apoptotic mechanisms mediated by SR-A are not fully understood. Therefore, we sought to see if SR-A mediated apoptosis was associated with autophagy in macrophages. Here, we showed that fucoidan inhibited microtubule-associated protein light chain 3-phospholipid conjugates (LC3-II) formation as well as the number of autophagosomes under ER stress. The inhibition of LC3-II formation was paralleled by the activation of the mTOR pathway, and the inhibition of mTOR allowed LC3-II induction in macrophages treated with thapsigargin plus fucoidan. Furthermore, apoptosis induced by fucoidan was prevented under ER stress by the mTOR inhibitor. We propose that fucoidan, a SR-A agonist, may contribute to macrophage apoptosis during ER stress by inhibiting autophagy.

Indexed as

apoptosisautophagyER stressmacrophageSR-A

Identifiers

PMID25013404
PMCPMC4085558
OpenAlexW2126938088

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.