Evidence map›Paper›PMID 22942739›Full record

Trial reportInternational journal of molecular sciences2012

Leukocyte mitochondrial DNA alteration in systemic lupus erythematosus and its relevance to the susceptibility to lupus nephritis.

Hui-Ting Lee, Chen-Sung Lin, Wei-Sheng Chen, Hsien-Tzung Liao, Chang-Youh Tsai, Yau-Huei Wei

Open access · goldAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  9. The role of mitochondria in rheumatic diseases.Nature reviews. Rheumatology · 2022
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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

6 authors at 2 institutions in 1 country.

Hui-Ting LeeInstitute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Chen-Sung LinInstitute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Wei-Sheng ChenInstitute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Hsien-Tzung LiaoDivision of Allergy, Immunology and Rheumatology, Department of Internal Medicine, Wan-Fang Hospital, Taipei Medical University, Taipei 116, Taiwan.
Chang-Youh TsaiInstitute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan.ORCID 0000-0002-4154-4018
Yau-Huei WeiInstitute of Clinical Medicine, National Yang-Ming University, Taipei 112, Taiwan.
National Yang Ming Chiao Tung University · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of mitochondrial DNA (mtDNA) alterations in the pathophysiology of systemic lupus erythematosus (SLE) remains unclear. We investigated sequence variations in the D310 region and copy number change of mtDNA in 85 SLE patients and 45 normal subjects. Leukocyte DNA and RNA were extracted from leukocytes of the peripheral venous blood. The D310 sequence variations and copy number of mtDNA, and mRNA expression levels of mtDNA-encoded genes in leukocytes were determined by quantitative real-time polymerase chain reaction (Q-PCR) and PCR-based direct sequencing, respectively. We found that leukocyte mtDNA in SLE patients exhibited higher frequency of D310 heteroplasmy (69.4% vs. 48.9%, p = 0.022) and more D310 variants (2.2 vs. 1.7, p = 0.014) than those found in controls. Among normal controls and patients with low, medium or high SLE disease activity index (SLEDAI), an ever-increasing frequency of D310 heteroplasmy was observed (p = 0.021). Leukocyte mtDNA copy number tended to be low in patients of high SLEDAI group (p = 0.068), especially in those harboring mtDNA with D310 heteroplasmy (p = 0.020). Moreover, the mtDNA copy number was positively correlated with the mRNA level of mtDNA-encoded ND1 (NADH dehydrogenase subunit 1) (p = 0.041) and ATPase 6 (ATP synthase subunit 6) (p = 0.030) genes. Patients with more D310 variants were more susceptible to lupus nephritis (p = 0.035). Taken together, our findings suggest that decrease in the mtDNA copy number and increase in D310 heteroplasmy of mtDNA are related to the development and progression of SLE, and that the patients harboring more D310 variants of mtDNA are more susceptible to lupus nephritis.

Indexed as

Gene Expression RegulationAdultDNA, MitochondrialHumansLeukocytesLupus NephritisMaleMiddle AgedMitochondrial ProteinsDNA, MitochondrialMitochondrial Proteinscopy numberD310 sequence variationheteroplasmymitochondrial DNAsystemic lupus erythematosus

Identifiers

PMID22942739
PMCPMC3430270
OpenAlexW2015097461

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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.