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Review
. 2023 Oct;238(10):2206-2227.
doi: 10.1002/jcp.31110. Epub 2023 Sep 2.

Biofactors regulating mitochondrial function and dynamics in podocytes and podocytopathies

Affiliations
Review

Biofactors regulating mitochondrial function and dynamics in podocytes and podocytopathies

Seyyedeh Mina Hejazian et al. J Cell Physiol. 2023 Oct.

Abstract

Podocytes are terminally differentiated kidney cells acting as the main gatekeepers of the glomerular filtration barrier; hence, inhibiting proteinuria. Podocytopathies are classified as kidney diseases caused by podocyte damage. Different genetic and environmental risk factors can cause podocyte damage and death. Recent evidence shows that mitochondrial dysfunction also contributes to podocyte damage. Understanding alterations in mitochondrial metabolism and function in podocytopathies and whether altered mitochondrial homeostasis/dynamics is a cause or effect of podocyte damage are issues that need in-depth studies. This review highlights the roles of mitochondria and their bioenergetics in podocytes. Then, factors/signalings that regulate mitochondria in podocytes are discussed. After that, the role of mitochondrial dysfunction is reviewed in podocyte injury and the development of different podocytopathies. Finally, the mitochondrial therapeutic targets are considered.

Keywords: diabetic nephropathy; mitochondrial dynamics; mitochondrial dysfunction; podocyte injury; podocytopathies.

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REFERENCES

    1. Abe, Y., Sakairi, T., Beeson, C., & Kopp, J. B. (2013). TGF-β1 stimulates mitochondrial oxidative phosphorylation and generation of reactive oxygen species in cultured mouse podocytes, mediated in part by the mTOR pathway. American Journal of Physiology-Renal Physiology, 305(10), F1477-F1490. https://doi.org/10.1152/ajprenal.00182.2013
    1. Abe, Y., Sakairi, T., Kajiyama, H., Shrivastav, S., Beeson, C., & Kopp, J. B. (2010). Bioenergetic characterization of mouse podocytes. American Journal of Physiology-Cell Physiology, 299(2), C464-C476. https://doi.org/10.1152/ajpcell.00563.2009
    1. Almeida, A., Almeida, J., Bolaños, J. P., & Moncada, S. (2001). Different responses of astrocytes and neurons to nitric oxide: The role of glycolytically generated ATP in astrocyte protection. Proceedings of the National Academy of Sciences, 98(26), 15294-15299. https://doi.org/10.1073/pnas.261560998
    1. Arif, E., Solanki, A. K., Srivastava, P., Rahman, B., Fitzgibbon, W. R., Deng, P., Budisavljevic, M. N., Baicu, C. F., Zile, M. R., Megyesi, J., Janech, M. G., Kwon, S. H., Collier, J., Schnellmann, R. G., & Nihalani, D. (2019). Mitochondrial biogenesis induced by the β2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury. Kidney International, 96(3), 656-673. https://doi.org/10.1016/j.kint.2019.03.023
    1. Ashraf, S., Gee, H. Y., Woerner, S., Xie, L. X., Vega-Warner, V., Lovric, S., Fang, H., Song, X., Cattran, D. C., Avila-Casado, C., Paterson, A. D., Nitschké, P., Bole-Feysot, C., Cochat, P., Esteve-Rudd, J., Haberberger, B., Allen, S. J., Zhou, W., Airik, R., … Hildebrandt, F. (2013). ADCK4 mutations promote steroid-resistant nephrotic syndrome through CoQ10 biosynthesis disruption. Journal of Clinical Investigation, 123(12), 5179-5189. https://doi.org/10.1172/jci69000

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