Gujarati 2020 Am J Physiol Renal Physiol

Gujarati NA, Vasquez JM, Bogenhagen DF, Mallipattu SK (2020) The complicated role of mitochondria in the podocyte. Am J Physiol Renal Physiol 319:F955-65. https://doi.org/10.1152/ajprenal.00393.2020

» [https://pubmed.ncbi.nlm.nih.gov/33073585/ PMID: 33073585 Open Access

Gujarati NA, Vasquez JM, Bogenhagen DF, Mallipattu SK (2020) Am J Physiol Renal Physiol

Abstract: Mitochondria play a complex role in maintaining cellular function including ATP generation, generation of biosynthetic precursors for macromolecules, maintenance of redox homeostasis, and metabolic waste management. Although the contribution of mitochondrial function in various kidney diseases has been studied, there are still avenues that need to be explored under healthy and diseased conditions. Mitochondrial damage and dysfunction have been implicated in experimental models of podocytopathy as well as in humans with glomerular diseases resulting from podocyte dysfunction. Specifically, in the podocyte, metabolism is largely driven by oxidative phosphorylation or glycolysis depending on the metabolic needs. These metabolic needs may change drastically in the presence of podocyte injury in glomerular diseases such as diabetic kidney disease or focal segmental glomerulosclerosis. Here, we review the role of mitochondria in the podocyte and the factors regulating its function at baseline and in a variety of podocytopathies to identify potential targets for therapy.

• Bioblast editor: Gnaiger E

Correction: FADH₂ and Complex II

FADH₂ is shown as the substrate feeding electrons into Complex II (CII). This is wrong and requires correction - for details see Gnaiger (2024).

Gnaiger E (2024) Complex II ambiguities ― FADH₂ in the electron transfer system. J Biol Chem 300:105470. https://doi.org/10.1016/j.jbc.2023.105470 - »Bioblast link«