Evidence map›Paper›PMID 33763168›Full record

ArticleOxidative medicine and cellular longevity2021

Melatonin Attenuates ox-LDL-Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling.

Peng Li, Changlian Xie, Jiankai Zhong, Zhongzhou Guo, Kai Guo, Qiuyun Tu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Melatonin amelioratesGenes & diseases · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Melatonin and Vascular Function.Antioxidants (Basel, Switzerland) · 2024
    Review
  11. Review
  12. The role and mechanisms of microvascular damage in the ischemic myocardium.Cellular and molecular life sciences : CMLS · 2023
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

6 authors at 4 institutions in 1 country.

Peng LiDepartment of Gerontology, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong Province 519000, China.ORCID https://orcid.org/0000-0002-3258-8975
Changlian XieIntensive Care Unit, The Traditional Chinese Medicine Hospital, Zhongshan, Guangdong Province 528400, China.
Jiankai ZhongDepartment of Cardiology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde), Foshan, Guangdong Province 528308, China.
Zhongzhou GuoDepartment of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong Province 510515, China.
Kai GuoCardiovascular Medicine Department, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong Province 510317, China.ORCID https://orcid.org/0000-0001-6354-6092
Qiuyun TuDepartment of Gerontology, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, Guangdong Province 519000, China.ORCID https://orcid.org/0000-0002-3215-3795
Sun Yat-sen University · CNGuangdong Provincial People's Hospital · CNNanfang Hospital · CNThe First People's Hospital of Shunde · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial dysfunction, which is characterized by damage to the endoplasmic reticulum (ER) and mitochondria, is involved in a variety of cardiovascular disorders. Here, we explored whether mitochondrial damage and ER stress are associated with endothelial dysfunction. We also examined whether and how melatonin protects against oxidized low-density lipoprotein- (ox-LDL-) induced damage in endothelial cells. We found that CHOP, GRP78, and PERK expressions, which are indicative of ER stress, increased significantly in response to ox-LDL treatment. ox-LDL also induced mitochondrial dysfunction as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS levels, and downregulation of mitochondrial protective factors. In addition, ox-LDL inhibited antioxidative processes, as evidenced by decreased antioxidative enzyme activity and reduced Nrf2/HO-1 expression. Melatonin clearly reduced ER stress and promoted mitochondrial function and antioxidative processes in the presence of ox-LDL. Molecular investigation revealed that ox-LDL activated the JNK/Mff signaling pathway, and melatonin blocked this effect. These results demonstrate that ox-LDL induces ER stress and mitochondrial dysfunction and activates the JNK/Mff signaling pathway, thereby contributing to endothelial dysfunction. Moreover, melatonin inhibited JNK/Mff signaling and sustained ER homeostasis and mitochondrial function, thereby protecting endothelial cells against ox-LDL-induced damage.

Indexed as

Signal TransductionEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHumansHuman Umbilical Vein Endothelial CellsJNK Mitogen-Activated Protein KinasesLipoproteins, LDLMelatoninMembrane ProteinsMitochondriaMitochondrial ProteinsOxidative StressEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanJNK Mitogen-Activated Protein KinasesLipoproteins, LDLMelatoninMembrane ProteinsMff protein, humanMitochondrial Proteinsoxidized low density lipoprotein

Identifiers

PMID33763168
PMCPMC7952160
OpenAlexW3134470983

What OpenQuestion holds

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LicenceCC BY
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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.