Evidence map›Paper›PMID 29456246›Full record

ReviewNature reviews. Nephrology2018

Mitochondrial dysfunction in diabetic kidney disease.

Josephine M Forbes, David R Thorburn

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 352 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
352citing papers in PubMed, 3 pooled it
26.8field-weighted citation impact, top 1% 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

352 citing papers in PubMed, 3 syntheses or guidelines pooled it, 604 citations in OpenAlex.

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292 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

2 authors at 2 institutions in 1 country.

Josephine M ForbesGlycation and Diabetes Group, Mater Research Institute, The University of Queensland, Translational Research Institute, Brisbane, Queensland, Australia.
David R ThorburnDepartments of Medicine and Paediatrics, The University of Melbourne, Parkville, Victoria, Australia.
Murdoch Children's Research Institute · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Globally, diabetes is the leading cause of chronic kidney disease and end-stage renal disease, which are major risk factors for cardiovascular disease and death. Despite this burden, the factors that precipitate the development and progression of diabetic kidney disease (DKD) remain to be fully elucidated. Mitochondrial dysfunction is associated with kidney disease in nondiabetic contexts, and increasing evidence suggests that dysfunctional renal mitochondria are pathological mediators of DKD. These complex organelles have a broad range of functions, including the generation of ATP. The kidneys are mitochondrially rich, highly metabolic organs that require vast amounts of ATP for their normal function. The delivery of metabolic substrates for ATP production, such as fatty acids and oxygen, is altered by diabetes. Changes in metabolic fuel sources in diabetes to meet ATP demands result in increased oxygen consumption, which contributes to renal hypoxia. Inherited factors including mutations in genes that impact mitochondrial function and/or substrate delivery may also be important risk factors for DKD. Hence, we postulate that the diabetic milieu and inherited factors that underlie abnormalities in mitochondrial function synergistically drive the development and progression of DKD.

Indexed as

AnimalsDiabetic NephropathiesDisease ProgressionHumansMitochondria

Identifiers

PMID29456246
OpenAlexW2788432017

What Socratic holds

Textmetadata
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 Socratic graph.