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

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

Research output: Contribution to journalReview articlepeer-review

1 Scopus citations

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.

Original languageEnglish (US)
Article number351
JournalBiomolecules
Volume12
Issue number3
DOIs
StatePublished - Mar 2022
Externally publishedYes

Keywords

  • Diabetic kidney disease
  • Mitochondrial dysfunction
  • Mitochondrial reactive oxygen species
  • Warburg effect

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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