Evidence map›Paper›PMID 35327540›Full record

ReviewBiomolecules2022

Glucose- and Non-Glucose-Induced Mitochondrial Dysfunction in Diabetic Kidney Disease.

Marie Ito, Margaret Zvido Gurumani, Sandra Merscher, Alessia Fornoni

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

Review in Biomolecules, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  16. [Linagliptin improves diabetic kidney disease in rats by promoting mitochondrial biogenesis through the AMPK/PGC-1Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023
    Article
  17. Review
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  19. SUPPRESION OF MITOCHONDRIAL RESPIRATION IS A FEATURE OF CELLULAR GLUCOSE TOXICITY.Transactions of the American Clinical and Climatological Association · 2023
    Article
  20. The Role of NLRP3 Inflammasome in IgA Nephropathy.Medicina (Kaunas, Lithuania) · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Marie ItoDepartment of Medicine, Katz Family Division of Nephrology and Hypertension, Peggy and Harold Katz Family Drug Discovery Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.ORCID 0000-0001-5515-2851
Margaret Zvido GurumaniDepartment of Medicine, Katz Family Division of Nephrology and Hypertension, Peggy and Harold Katz Family Drug Discovery Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Sandra MerscherDepartment of Medicine, Katz Family Division of Nephrology and Hypertension, Peggy and Harold Katz Family Drug Discovery Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
Alessia FornoniDepartment of Medicine, Katz Family Division of Nephrology and Hypertension, Peggy and Harold Katz Family Drug Discovery Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA.
University of Miami · US

Funding

Miami Clinical Translational Science Institute U54DK083912, UM1DK100846, U01DK116101 and UL1TR000460NIH HHS R01DK117599, R01DK104753 and R01CA227493
6 · The paper itself

Abstract

Mitochondrial dysfunction plays an important role in the pathogenesis and progression of diabetic kidney disease (DKD). In this review, we will discuss mitochondrial dysfunction observed in preclinical models of DKD as well as in clinical DKD with a focus on oxidative phosphorylation (OXPHOS), mitochondrial reactive oxygen species (mtROS), biogenesis, fission and fusion, mitophagy and urinary mitochondrial biomarkers. Both glucose- and non-glucose-induced mitochondrial dysfunction will be discussed. In terms of glucose-induced mitochondrial dysfunction, the energetic shift from OXPHOS to aerobic glycolysis, called the Warburg effect, occurs and the resulting toxic intermediates of glucose metabolism contribute to DKD-induced injury. In terms of non-glucose-induced mitochondrial dysfunction, we will review the roles of lipotoxicity, hypoxia and vasoactive pathways, including endothelin-1 (Edn1)/Edn1 receptor type A signaling pathways. Although the relative contribution of each of these pathways to DKD remains unclear, the goal of this review is to highlight the complexity of mitochondrial dysfunction in DKD and to discuss how markers of mitochondrial dysfunction could help us stratify patients at risk for DKD.

Indexed as

Diabetes MellitusDiabetic NephropathiesBiomarkersFemaleGlucoseHumansMaleMitochondriaReactive Oxygen SpeciesBiomarkersGlucoseReactive Oxygen Speciesdiabetic kidney diseasemitochondrial dysfunctionmitochondrial reactive oxygen speciesWarburg effect

Identifiers

PMID35327540
PMCPMC8945149
OpenAlexW4213226632

What OpenQuestion holds

Textmetadata
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.