Evidence map›Paper›PMID 34077894›Full record

ArticleRedox biology2021

Lutein attenuates angiotensin II- induced cardiac remodeling by inhibiting AP-1/IL-11 signaling.

Youming Chen, Lan Wang, Shixing Huang, Jiangfeng Ke, Qing Wang, Zhiwen Zhou, Wei Chang

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
8.5field-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

31 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Fibroblast-derived interleukin-6 exacerbates adverse cardiac remodeling after myocardial infarction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024
    Article
  18. Review
  19. Article
  20. 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

7 authors at 3 institutions in 1 country.

Youming ChenDepartment of Cardiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Lan WangDepartment of Radiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Shixing HuangDepartment of Cardiovascular Surgery, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Jiangfeng KeDepartment of Endocrinology and metabolism, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Qing WangDepartment of Traditional Chinese Medicine, Shanghai Jiaotong University Affiliated Sixth People's Hospital, Shanghai, China.
Zhiwen ZhouDepartment of Cardiology, Shanghai Xuhui District Central Hospital & Zhongshan-xuhui Hospital, Shanghai, China. Electronic address: zhouzhiwenufo@sina.com.
Wei ChangDepartment of Emergency, Shanghai Xuhui District Central Hospital & Zhongshan-xuhui Hospital, Shanghai, China. Electronic address: changwei1st@163.com.
Shanghai Sixth People's Hospital · CNRuijin Hospital · CNShanghai Xuhui Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleOxidative stress plays a critical role in the development of cardiac remodeling and heart failure. Lutein, the predominant nonvitamin A carotenoid, has been shown to have profound effects on oxidative stress. However, the effect of lutein on angiotensin II (Ang II)-induced cardiac remodeling and heart failure remains unknown.

objectiveThe aim of this study was to determine whether lutein is involved in cardiac remodeling and to elucidate the underlying molecular mechanisms. METHODS AND

resultsIn vitro experiments with isolated neonatal rat cardiomyocytes (NRCMs) and cardiac fibroblasts (CFs) revealed that lutein significantly attenuated Ang II-induced collagen expression in CFs, and cardiomyocyte hypertrophy. The Ang II-induced increases in superoxide generation, inflammation and apoptosis in cultured CFs were strikingly prevented by lutein. In vivo, fibrosis, hypertrophic cardiomyocyte and superoxide generation were analyzed, and lutein was demonstrated to confer resistance to Ang II-induced cardiac remodeling in mice. Mechanistically, RNA sequencing revealed that interleukin-11 (IL-11) expression was significantly upregulated in mouse hearts in response to Ang II infusion and was significantly suppressed in the hearts of lutein-treated mice. Furthermore, IL-11 overexpression blocked the effects of lutein on fibrosis and oxidative stress in CFs and impaired the protective effect of lutein on cardiac remodeling. Notably, we discovered that lutein could reduce Ang II-induced IL-11 expression, at least partly through the regulation of activator protein (AP)-1 expression and activity.

conclusionsLutein has potential as a treatment for cardiac remodeling and heart failure via the suppression of IL-11 expression.

Indexed as

Angiotensin IITranscription Factor AP-1AnimalsCardiomegalyFibrosisInterleukin-11LuteinMiceMice, Inbred C57BLMyocardiumRatsVentricular RemodelingAngiotensin IIInterleukin-11LuteinTranscription Factor AP-1AP-1Cardiac fibrosisCardiac remodelingIL-11Lutein

Identifiers

PMID34077894
PMCPMC8181194
OpenAlexW3165206923

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.