Evidence map›Paper›PMID 28698385›Full record

ArticleThe Journal of biological chemistry2017

Retinoic acid receptor-related orphan receptor α stimulates adipose tissue inflammation by modulating endoplasmic reticulum stress.

Yin Liu, Yulong Chen, Jinlong Zhang, Yulan Liu, Yanjie Zhang, Zhiguang Su

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 45 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Yin LiuFrom the Molecular Medicine Research Center, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan, China.
Yulong ChenFrom the Molecular Medicine Research Center, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan, China.
Jinlong ZhangFrom the Molecular Medicine Research Center, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan, China.
Yulan LiuFrom the Molecular Medicine Research Center, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan, China.
Yanjie ZhangFrom the Molecular Medicine Research Center, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan, China.
Zhiguang SuFrom the Molecular Medicine Research Center, West China Hospital, State Key Laboratory of Biotherapy, Sichuan University, Chengdu 610041, Sichuan, China. Electronic address: zhiguang.su@scu.edu.cn.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adipose tissue inflammation has been linked to metabolic diseases such as obesity and type 2 diabetes. However, the molecules that mediate inflammation in adipose tissue have not been addressed. Although retinoic acid receptor-related orphan receptor α (RORα) is known to be involved in the regulation of inflammatory response in some tissues, its role is largely unknown in adipose tissue. Conversely, it is known that endoplasmic reticulum (ER) stress and unfolding protein response (UPR) signaling affect the inflammatory response in obese adipose tissue, but whether RORα regulates these processes remains unknown. In this study, we investigate the link between RORα and adipose tissue inflammation. We showed that the inflammatory response in macrophages or 3T3-L1 adipocytes stimulated by lipopolysaccharide, as well as adipose tissue in obese mice, markedly increased the expression of RORα. Adenovirus-mediated overexpression of RORα or treatment with the RORα-specific agonist SR1078 enhanced the expression of inflammatory cytokines and increased the number of infiltrated macrophages into adipose tissue. Furthermore, SR1078 up-regulated the mRNA expression of ER stress response genes and enhanced phosphorylations of two of the three mediators of major UPR signaling pathways, PERK and IRE1α. Finally, we found that alleviation of ER stress using a chemical chaperone followed by the suppression of RORα induced inflammation in adipose tissue. Our data suggest that RORα-induced ER stress response potentially contributes to the adipose tissue inflammation that can be mitigated by treatment with chemical chaperones. The relationships established here between RORα expression, inflammation, and UPR signaling may have implications for therapeutic targeting of obesity-related metabolic diseases.

Indexed as

Endoplasmic Reticulum StressUnfolded Protein Response3T3-L1 CellsAdipocytes, WhiteAnimalsAnti-Obesity AgentsBenzamidesFluorocarbonsGene Expression RegulationInsulin ResistanceLipopolysaccharidesMacrophage ActivationMacrophagesMaleMiceMice, Inbred C57BL4-phenylbutyric acidAnti-Obesity AgentsBenzamidesFluorocarbonsLipopolysaccharidesNuclear Receptor Subfamily 1, Group F, Member 1PhenylbutyratesRecombinant ProteinsRora protein, mouseSR 1078adipocyteadipose tissueendoplasmic reticulum stress (ER stress)inflammationobesityRORα

Identifiers

PMID28698385
PMCPMC5572914
OpenAlexW2734490723

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.