Evidence map›Paper›PMID 31504769›Full record

ArticleNucleic acids research2019

Hypertension-associated mitochondrial DNA 4401A>G mutation caused the aberrant processing of tRNAMet, all 8 tRNAs and ND6 mRNA in the light-strand transcript.

Xiaoxu Zhao, Limei Cui, Yun Xiao, Qin Mao, Maerhaba Aishanjiang, Wanzhong Kong, Yuqi Liu, Hong Chen, Fang Hong, Zidong Jia and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

  1. Hypertensive mt. tRNARedox biology · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. RNase P: Beyond Precursor tRNA Processing.Genomics, proteomics & bioinformatics · 2024
    Review
  8. Clinical and genetic analysis of essential hypertension with mitochondrial tRNAZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024
    Article
  9. Clinical and genetic analysis of essential hypertension withZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Article
  10. Novel mitochondrial tRNAIrish journal of medical science · 2023
    Article
  11. Mitophagy in hypertension-mediated organ damage.Frontiers in cardiovascular medicine · 2023
    Review
  12. Review
  13. The Mitochondrial tRNAFrontiers in genetics · 2022
    Article
  14. Article
  15. Article
  16. Article
  17. 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

13 authors at 5 institutions in 1 country.

Xiaoxu ZhaoDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Limei CuiDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Yun XiaoDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Qin MaoInstitute of Genetics, and Department of Human Genetics, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Maerhaba AishanjiangInstitute of Genetics, and Department of Human Genetics, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Wanzhong KongDepartment of Clinical Laboratory, Wenzhou Traditional Chinese Medicine Hospital, Wenzhou, Zhejiang 325000, China.
Yuqi LiuCardiac Department, Chinese PLA General Hospital, Beijing 100853, China.
Hong ChenEmergy Medicine Department, Ningbo First Hospital, Zhejiang University School of Medicine, Ningbo, Zhejiang 315000, China.
Fang HongDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Zidong JiaDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Meng WangDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Pingping JiangDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Min-Xin GuanDivision of Medical Genetics and Genomics, The Children's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, China.
Children's Hospital of Zhejiang University · CNZhejiang University · CNChinese PLA General Hospital · CNNingbo First Hospital · CNWenzhou Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial tRNA processing defects were associated with human diseases but their pathophysiology remains elusively. The hypertension-associated m.4401A>G mutation resided at a spacer between mitochondrial tRNAMet and tRNAGln genes. An in vitro processing experiment revealed that the m.4401A>G mutation caused 59% and 69% decreases in the 5' end processing efficiency of tRNAGln and tRNAMet precursors, catalyzed by RNase P, respectively. Using human umbilical vein endothelial cells-derived cybrids, we demonstrated that the m.4401A>G mutation caused the decreases of all 8 tRNAs and ND6 and increases of longer and uncleaved precursors from the Light-strand transcript. Conversely, the m.4401A>G mutation yielded the reduced levels of tRNAMet level but did not change the levels of other 13 tRNAs, 12 mRNAs including ND1, 12S rRNA and 16S rRNA from the Heavy-strand transcript. These implicated the asymmetrical processing mechanisms of H-strand and L-strand polycistronic transcripts. The tRNA processing defects play the determined roles in the impairing mitochondrial translation, respiratory deficiency, diminishing membrane potential, increasing production of reactive oxygen species and altering autophagy. Furthermore, the m.4401A>G mutation altered the angiogenesis, evidenced by aberrant wound regeneration and weaken tube formation in mutant cybrids. Our findings provide new insights into the pathophysiology of hypertension arising from mitochondrial tRNA processing defects.

Indexed as

Transcription, GeneticDNA, MitochondrialHumansHuman Umbilical Vein Endothelial CellsHypertensionMutationNADH DehydrogenaseRNA Processing, Post-TranscriptionalRNA, RibosomalRNA, Ribosomal, 16SRNA, Transfer, GlnRNA, Transfer, MetDNA, MitochondrialMT-ND6 protein, humanNADH DehydrogenaseNADH dehydrogenase subunit 1, humanRNA, RibosomalRNA, ribosomal, 12SRNA, Ribosomal, 16SRNA, Transfer, GlnRNA, Transfer, Met

Identifiers

PMID31504769
PMCPMC6821173
OpenAlexW2970275031

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.