Evidence map›Paper›PMID 35646539›Full record

ArticleActa pharmaceutica Sinica. B2022

Autophagy enhanced by curcumin ameliorates inflammation in atherogenesis

Xuesong Li, Ruigong Zhu, Hong Jiang, Quanwen Yin, Jiaming Gu, Jiajing Chen, Xian Ji, Xuan Wu, Haiping Fu, Hui Wang and 5 more

Open access · diamondAbstract read
In one paragraph

Article in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 119 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
  5. Inhibition of PI3K/Akt/mTOR signaling by curcumin: a novel approach to mitigate synovial fibrosis in knee osteoarthritis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Review
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  12. Article
  13. Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026
    Review
  14. Review
  15. Review
  16. Review
  17. Lipid metabolism in homeostasis and disease.Signal transduction and targeted therapy · 2026
    Review
  18. Review
  19. Article
  20. Review

19 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Xuesong LiKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Ruigong ZhuKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Hong JiangKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Quanwen YinKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Jiaming GuKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Jiajing ChenKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Xian JiKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Xuan WuKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Haiping FuKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Hui WangKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Xin TangKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Yuanqing GaoKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Bingjian WangDepartment of Cardiology, Huai'an First People's Hospital Affiliated with Nanjing Medical University, Huai'an 223399, China.
Yong JiKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Hongshan ChenKey Laboratory of Cardiovascular and Cerebrovascular Medicine, School of Pharmacy, Nanjing Medical University, Nanjing 211166, China.
Nanjing Medical University · CNHuaian First People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disturbance of macrophage-associated lipid metabolism plays a key role in atherosclerosis. Crosstalk between autophagy deficiency and inflammation response in foam cells (FCs) through epigenetic regulation is still poorly understood. Here, we demonstrate that in macrophages, oxidized low-density lipoprotein (ox-LDL) leads to abnormal crosstalk between autophagy and inflammation, thereby causing aberrant lipid metabolism mediated through a dysfunctional transcription factor EB (TFEB)-P300-bromodomain-containing protein 4 (BRD4) axis. ox-LDL led to macrophage autophagy deficiency along with TFEB cytoplasmic accumulation and increased reactive oxygen species generation. This activated P300 promoted BRD4 binding on the promoter regions of inflammatory genes, consequently contributing to inflammation with atherogenesis. Particularly, ox-LDL activated BRD4-dependent super-enhancer associated with liquid-liquid phase separation (LLPS) on the regulatory regions of inflammatory genes. Curcumin (Cur) prominently restored FCs autophagy by promoting TFEB nuclear translocation, optimizing lipid catabolism, and reducing inflammation. The consequences of P300 and BRD4 on super-enhancer formation and inflammatory response in FCs could be prevented by Cur. Furthermore, the anti-atherogenesis effect of Cur was inhibited by macrophage-specific

Indexed as

Acetyl-H3, acetyl-histone 3ATG5, autophagy-related 5AtherosclerosisAutophagyBET, bromodomain and extra-terminalBRD4BRD4, bromodomain protein 4ChIP, chromatin immunoprecipitationCQ, chloroquineCurcuminCur, curcuminCVDs, cardiovascular diseasesDil-ox-LDL, 1,1′-dioctadecyl-3,3,3′,3′-tetramethy-lindocarbocyanine perchlorate labeled oxidized low-density lipoproteinFCs, foam cellsHFD, high-fat dietIL-1β, interleukin 1βInflammationLIR, LC3-interacting regionMacrophageMCP-1, monocyte chemotactic protein 1mTORC1, mammalian target of rapamycin complex 1NAC, N-acetyl-l-cysteineORO, Oil red Oox-LDL, oxidized low-density lipoproteinP300qRT-PCR, quantitative real-time polymerase chain reactionRe-ChIP, re-chromatin immunoprecipitationROS, reactive oxygen speciesSE, super-enhancersiRNAs, small interference RNAsTFEBTFEB, transcription factor EBTNF-α, tumor necrosis factor α

Identifiers

PMID35646539
PMCPMC9136579
OpenAlexW4200110434

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.