Evidence map›Paper›PMID 29311972›Full record

ArticleFrontiers in physiology2017

Astaxanthin Attenuates Homocysteine-Induced Cardiotoxicity

Cun-Dong Fan, Jing-Yi Sun, Xiao-Ting Fu, Ya-Jun Hou, Yuan Li, Ming-Feng Yang, Xiao-Yan Fu, Bao-Liang Sun

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Astaxanthin Protects Against HLife (Basel, Switzerland) · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. MiRZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

8 authors at 3 institutions in 2 countries.

Cun-Dong FanKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Jing-Yi SunWonju Severance Christian Hospital, Yonsei University Wonju College of Medicine, Wonju, South Korea.
Xiao-Ting FuKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Ya-Jun HouKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Yuan LiKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Ming-Feng YangKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Xiao-Yan FuKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Bao-Liang SunKey Lab of Cerebral Microcirculation in Universities of Shandong, Taishan Medical University, Taian, China.
Taishan Medical University · CNAffiliated Hospital of Taishan Medical University · CNYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homocysteine (Hcy) as an independent risk factor contributes to the occurrence and development of human cardiovascular diseases (CVD). Induction of oxidative stress and apoptosis was commonly accepted as the major mechanism in Hcy-induced cardiotoxicity. Astaxanthin (ATX) as one of the most powerful antioxidants exhibits novel cardioprotective potential against Hcy-induced endothelial dysfunction. However, the protective effect and mechanism of ATX against Hcy-induced cardiotoxicity in cardiomyocytes have not been elucidated yet. Herein, H9c2 rat cardiomyocytes and Hcy-injured animal model were employed in the present study. The MTT, flow cytometry analysis (FCM), TUNEL-DAPI and western blotting results all demonstrated that ATX significantly alleviated Hcy-induced cytotoxicity in H9c2 cells through inhibition of mitochondria-mediated apoptosis. The JC-1 and Mito-tracker staining both revealed that ATX pre-treatment blocked Hcy-induced mitochondrial dysfunction by regulating Bcl-2 family expression. Moreover, DCFH-DA and Mito-SOX staining showed that ATX effectively attenuated Hcy-induced oxidative damage via scavenging intracellular reactive oxygen species (ROS). Importantly, the ELISA and immunohistochemical results indicated that Hcy-induced cardiotoxicity

Indexed as

astaxanthincardiovascular diseaseshomocysteinemitochondrial dysfunctionoxidative damage

Identifiers

PMID29311972
PMCPMC5733103
OpenAlexW2773292660

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.