Evidence map›Paper›PMID 31959742›Full record

ArticleCell death & disease2020

Hypermethylation of mitochondrial DNA in vascular smooth muscle cells impairs cell contractility.

Yue-Feng Liu, Juan-Juan Zhu, Xiao Yu Tian, Han Liu, Tao Zhang, Yun-Peng Zhang, Si-An Xie, Ming Zheng, Wei Kong, Wei-Juan Yao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Polygonum cuspidatum Exosome-Like Nanovesicles Alleviate Hypoxic Pulmonary Hypertension by Stabilizing PON1 to Inhibit MAPK-Mediated PASMC Phenotypic Switching.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
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  13. The uteroplacental circulation at high altitude: adaptation and maladaptation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
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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

14 authors at 4 institutions in 1 country.

Yue-Feng Liu *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Juan-Juan Zhu *Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Xiao Yu TianSchool of Biomedical Sciences, Institute of Vascular Medicine, CUHK Shenzhen Research Institute, Chinese University of Hong Kong, Hong Kong, People's Republic of China.
Han LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Tao ZhangDepartment of Vascular Surgery, Peking University People's Hospital, Beijing, People's Republic of China.
Yun-Peng ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Si-An XieDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Ming ZhengDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Wei KongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Wei-Juan YaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Wei PangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Chuan-Rong ZhaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Yuan-Jun TangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China.
Jing ZhouDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing, People's Republic of China. jzhou@bjmu.edu.cn.
Ministry of Education of the People's Republic of China · CNPeking University · CNChinese University of Hong Kong, Shenzhen · CNPeking University People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular smooth muscle cell (SMC) from arterial stenotic-occlusive diseases is featured with deficiency in mitochondrial respiration and loss of cell contractility. However, the regulatory mechanism of mitochondrial genes and mitochondrial energy metabolism in SMC remains elusive. Here, we described that DNA methyltransferase 1 (DNMT1) translocated to the mitochondria and catalyzed D-loop methylation of mitochondrial DNA in vascular SMCs in response to platelet-derived growth factor-BB (PDGF-BB). Mitochondrial-specific expression of DNMT1 repressed mitochondrial gene expression, caused functional damage, and reduced SMC contractility. Hypermethylation of mitochondrial D-loop regions were detected in the intima-media layer of mouse carotid arteries subjected to either cessation of blood flow or mechanical endothelial injury, and also in vessel specimens from patients with carotid occlusive diseases. Likewise, the ligated mouse arteries exhibited an enhanced mitochondrial binding of DNMT1, repressed mitochondrial gene expression, defects in mitochondrial respiration, and impaired contractility. The impaired contractility of a ligated vessel could be restored by ex vivo transplantation of DNMT1-deleted mitochondria. In summary, we discovered the function of DNMT1-mediated mitochondrial D-loop methylation in the regulation of mitochondrial gene transcription. Methylation of mitochondrial D-loop in vascular SMCs contributes to impaired mitochondrial function and loss of contractile phenotype in vascular occlusive disease.

Indexed as

AnimalsBecaplerminCell NucleusCell RespirationDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationDNA, MitochondrialFemaleGene Expression RegulationHumansMaleMice, Inbred C57BLMitochondriaMuscle, Smooth, VascularMyocytes, Smooth MuscleVascular DiseasesBecaplerminDNA (Cytosine-5-)-Methyltransferase 1DNA, MitochondrialDNMT1 protein, human

Identifiers

PMID31959742
PMCPMC6971246
OpenAlexW3000483740

What OpenQuestion holds

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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.