Evidence map›Paper›PMID 33886081›Full record

ArticleJournal of physiology and biochemistry2021

Autophagy blockage promotes the pyroptosis of ox-LDL-treated macrophages by modulating the p62/Nrf2/ARE axis.

Jiaru Liu, Chao Wang, Jiashan Li, Ying Yu, Yuee Liu, Huihui Liu, Qi Peng, Xiuru Guan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of physiology and biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

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  20. The Interplay Between Autophagy and Regulated Necrosis.Antioxidants & redox signaling · 2023
    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.

Jiaru LiuDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Chao WangDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Jiashan LiDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Ying YuDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Yuee LiuDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Huihui LiuDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Qi PengDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China.
Xiuru GuanDepartment of Laboratory Diagnostics, the First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, NanGang, Harbin, Heilongjiang, 150001, People's Republic of China. gxr0451@sina.com.ORCID http://orcid.org/0000-0001-6024-059X
Harbin Medical University · CN

Funding

National Natural Science Foundation of China 81672084
6 · The paper itself

Abstract

Atherosclerosis, a chronic comprehensive cardiovascular disease, is characterized by the lipid infiltration, formation of foam cells derived from macrophages and inflammation in the vessel wall. Substantial evidence confirms that the activity of autophagic bodies plays a pivot role in regulating cell deaths, but the mechanisms of autophagy to regulate the pyroptosis of macrophages in atherosclerosis remain unclear. In our study, we explored that ox-LDL decreased the cell viability and destroyed the integrity of cell membrane, resulting in the pyroptosis of THP-1 derived macrophages in a dose-dependent manner. Western blotting, qRT-PCR and ELISA also showed that chloroquine (CQ) could up-regulate the expression of p62 through impairing autophagy and induce the pyroptosis of macrophages treated by ox-LDL, as evidenced by the decrease of cell viability and membrane integrity, and the increase of pro-caspase-1, GSDMD, and proinflammatory factors IL-1β and IL-18. Further researches demonstrated that Nrf2, a nuclear factor activated by p62, was linked to macrophage pyroptosis. Overactivating or suppressing Nrf2/ARE signaling would correspondingly aggravate or alleviate pyroptosis, in which the level of p62 was regulated by Nrf2 feedback. Then, bioinformatic analysis verified that there was a close interaction between p62, Nrf2/ARE signaling proteins and pyroptosis-related proteins. Taken together, our results show that blocking autophagy promotes the pyroptosis of ox-LDL-treated macrophages via the p62/Nrf2/ARE axis, providing a novel therapeutic target for atherosclerosis.

Indexed as

AutophagyPyroptosisAtherosclerosisHumansMacrophagesNF-E2-Related Factor 2RNA-Binding ProteinsTHP-1 CellsNFE2L2 protein, humanNF-E2-Related Factor 2P62 protein, humanRNA-Binding ProteinsAtherosclerosisAutophagyNrf2/ARE pathwayPyroptosis

Identifiers

PMID33886081
PMCPMC8060691
OpenAlexW3154208825

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.