Evidence map›Paper›PMID 35138251›Full record

ArticleeLife2022

Covalent inhibition of endoplasmic reticulum chaperone GRP78 disconnects the transduction of ER stress signals to inflammation and lipid accumulation in diet-induced obese mice.

Dan Luo, Ni Fan, Xiuying Zhang, Fung Yin Ngo, Jia Zhao, Wei Zhao, Ming Huang, Ding Li, Yu Wang, Jianhui Rong

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  13. The role of celastrol in inflammation and diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Current neuropharmacology · 2024
    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

10 authors at 3 institutions in 2 countries.

Dan Luo *School of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Ni Fan *School of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Xiuying ZhangSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Fung Yin NgoSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Jia ZhaoSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Wei ZhaoSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Ming HuangDepartment of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Ding LiColleage of Chemistry and Pharmacy, College of Chemistry & Pharmacy, Northwest A&F University, Shaanxi, China.
Yu WangDepartment of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.
Jianhui RongSchool of Chinese Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China.ORCID 0000-0002-3545-2811
Chinese University of Hong Kong · HKUniversity of Hong Kong · HKNorthwest A&F University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting endoplasmic reticulum (ER) stress, inflammation, and metabolic dysfunctions may halt the pathogenesis of obesity and thereby reduce the prevalence of diabetes, cardiovascular disesases, and cancers. The present study was designed to elucidate the mechnaisms by which plant-derived celastrol ameliorated inflammation and lipid accumulation in obesity. The mouse model of diet-induced obesity was induced by feeding high-fat diet for 3 months and subsequently intervented with celastrol for 21 days. Hepatic and adipose tissues were analyzed for lipid accumulation, macrophage activation, and biomarker expression. As result, celastrol effectively reduced body weight, suppressed ER stress, inflammation, and lipogenesis while promoted hepatic lipolysis. RNA-sequencing revealed that celastrol-loaded nanomicelles restored the expression of 49 genes that regulate ER stress, inflammation, and lipid metabolism. On the other hand, celastrol-PEG4-alkyne was synthesized for identifying celastrol-bound proteins in RAW264.7 macrophages. ER chaperone GRP78 (78 kDa glucose-regulated protein) was identified by proteomics approach for celastrol binding to the residue Cys

Indexed as

Insulin ResistanceAdipose TissueAnimalsDiet, High-FatEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressInflammationLipid MetabolismLiverMacrophage ActivationMacrophagesMaleMiceMice, Inbred C57BLMice, ObeseObesitycelastrolEndoplasmic Reticulum Chaperone BiPHspa5 protein, mousePentacyclic Triterpenesbiochemistrycelastrolchemical biologyER stressGRP78inflammationlipid accumulationmedicinemouseobesity

Identifiers

PMID35138251
PMCPMC8828050
OpenAlexW4220976166

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.