Evidence map›Paper›PMID 26288815›Full record

ArticleEBioMedicine2015

Altered Mitochondrial Function, Mitochondrial DNA and Reduced Metabolic Flexibility in Patients With Diabetic Nephropathy.

Anna Czajka, Saima Ajaz, Luigi Gnudi, Chandani Kiran Parsade, Peter Jones, Fiona Reid, Afshan N Malik

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

116 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.

  1. Pooled it
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  8. Therapeutic Potential of Mitochondrial Transplantation with Focus on DBD.International journal of molecular sciences · 2026
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56 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Anna CzajkaDiabetes Research Group, Division of Diabetes and Nutritional Science, Faculty of Life Sciences and Medicine, King's College London, SE1 1UL, UK.
Saima AjazDiabetes Research Group, Division of Diabetes and Nutritional Science, Faculty of Life Sciences and Medicine, King's College London, SE1 1UL, UK.
Luigi GnudiCardiovascular Division.
Chandani Kiran ParsadeDiabetes Research Group, Division of Diabetes and Nutritional Science, Faculty of Life Sciences and Medicine, King's College London, SE1 1UL, UK.
Peter JonesDiabetes Research Group, Division of Diabetes and Nutritional Science, Faculty of Life Sciences and Medicine, King's College London, SE1 1UL, UK.
Fiona ReidDepartment of Primary Care and Public Health Sciences.
Afshan N MalikDiabetes Research Group, Division of Diabetes and Nutritional Science, Faculty of Life Sciences and Medicine, King's College London, SE1 1UL, UK.
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of this study was to determine if mitochondrial dysfunction plays a role in diabetic nephropathy (DN), a kidney disease which affects > 100 million people worldwide and is a leading cause of renal failure despite therapy. A cross-sectional study comparing DN with diabetes patients without kidney disease (DC) and healthy controls (HCs); and renal mesangial cells (HMCs) grown in normal and high glucose, was carried out. Patients with diabetes (DC) had increased circulating mitochondrial DNA (MtDNA), and HMCs increased their MtDNA within 24 h of hyperglycaemia. The increased MtDNA content in DCs and HMCs was not functional as transcription was unaltered/down-regulated, and MtDNA damage was present. MtDNA was increased in DC compared to HC, conversely, patients with DN had lower MtDNA than DC. Hyperglycaemic HMCs had fragmented mitochondria and TLR9 pathway activation, and in diabetic patients, mitophagy was reduced. Despite MtDNA content and integrity changing within 4 days, hyperglycaemic HMCs had a normal bio-energetic profile until 8 days, after which mitochondrial metabolism was progressively impaired. Peripheral blood mononuclear cells (PBMCs) from DN patients had reduced reserve capacity and maximal respiration, loss of metabolic flexibility and reduced Bioenergetic Health Index (BHI) compared to DC. Our data show that MtDNA changes precede bioenergetic dysfunction and that patients with DN have impaired mitochondrial metabolism compared to DC, leading us to propose that systemic mitochondrial dysfunction initiated by glucose induced MtDNA damage may be involved in the development of DN. Longitudinal studies are needed to define a potential cause-effect relationship between changes in MtDNA and bioenergetics in DN.

Indexed as

Cells, CulturedCross-Sectional StudiesDiabetes MellitusDiabetic NephropathiesDNA, MitochondrialEnergy MetabolismEnzyme ActivationGlucoseHumansHyperglycemiaLeukocytes, MononuclearMesangial CellsMitochondriaMitophagyToll-Like Receptor 9DNA, MitochondrialGlucoseTLR9 protein, humanToll-Like Receptor 9Bioenergetic deficitBioenergetic health index (BHI)Diabetic nephropathyHyperglycemiaMitochondrial DNAMitochondrial dysfunction

Identifiers

PMID26288815
PMCPMC4534759
OpenAlexW2017284901

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.