Evidence map›Paper›PMID 39152196›Full record

ArticleCommunications biology2024

Rhein targets macrophage SIRT2 to promote adipose tissue thermogenesis in obesity in mice.

Ruo-Nan Zhou, Zi-Wei Zhu, Ping-Yuan Xu, Li-Xuan Shen, Ziwei Wang, Ying-Ying Xue, Ying-Ying Xiang, Yue Cao, Xi-Zhong Yu, Juan Zhao and 5 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

15 authors.

Ruo-Nan ZhouDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.ORCID 0000-0002-6861-9411
Zi-Wei ZhuDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Ping-Yuan XuDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Li-Xuan ShenDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Ziwei WangDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Ying-Ying XueDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Ying-Ying XiangDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Yue CaoDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Xi-Zhong YuKey Laboratory for Metabolic Diseases in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Juan ZhaoKey Laboratory for Metabolic Diseases in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Yu JinKey Laboratory for Metabolic Diseases in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Jing YanKey Laboratory for Metabolic Diseases in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China.
Qin YangDepartment of Medicine, Physiology and Biophysics, University of California, Irvine, CA, 92697, USA.
Peng-Hua FangKey Laboratory for Metabolic Diseases in Chinese Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. fphlcollegesci@njucm.edu.cn.ORCID 0000-0002-8915-0616
Wen-Bin ShangDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, the Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210029, China. wbshang@njucm.edu.cn.ORCID 0000-0002-0317-5928

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rhein, a component derived from rhubarb, has been proven to possess anti-inflammatory properties. Here, we show that rhein mitigates obesity by promoting adipose tissue thermogenesis in diet-induced obese mice. We construct a macrophage-adipocyte co-culture system and demonstrate that rhein promotes adipocyte thermogenesis through inhibiting NLRP3 inflammasome activation in macrophages. Moreover, clues from acetylome analysis identify SIRT2 as a potential drug target of rhein. We further verify that rhein directly interacts with SIRT2 and inhibits NLRP3 inflammasome activation in a SIRT2-dependent way. Myeloid knockdown of SIRT2 abrogates adipose tissue thermogenesis and metabolic benefits in obese mice induced by rhein. Together, our findings elucidate that rhein inhibits NLRP3 inflammasome activation in macrophages by regulating SIRT2, and thus promotes white adipose tissue thermogenesis during obesity. These findings uncover the molecular mechanism underlying the anti-inflammatory and anti-obesity effects of rhein, and suggest that rhein may become a potential drug for treating obesity.

Indexed as

AnthraquinonesMacrophagesObesitySirtuin 2ThermogenesisAdipocytesAdipose TissueAnimalsInflammasomesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinAnthraquinonesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinrheinSirt2 protein, mouseSirtuin 2

Identifiers

PMID39152196
PMCPMC11329635

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.