Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Redox Metabolism and Vascular Calcification in Chronic-Kidney Disease

Version 1 : Received: 24 July 2023 / Approved: 25 July 2023 / Online: 26 July 2023 (02:38:33 CEST)

A peer-reviewed article of this Preprint also exists.

Carrillo-López, N.; Panizo, S.; Martín-Carro, B.; Mayo Barrallo, J.C.; Román-García, P.; García-Castro, R.; Fernández-Gómez, J.M.; Hevia-Suárez, M.Á.; Martín-Vírgala, J.; Fernández-Villabrille, S.; Martínez-Arias, L.; Vázquez, S.B.; Calleros Basilio, L.; Naves-Díaz, M.; Cannata-Andía, J.B.; Quirós-González, I.; Alonso-Montes, C.; Fernández-Martín, J.L. Redox Metabolism and Vascular Calcification in Chronic Kidney Disease. Biomolecules 2023, 13, 1419. Carrillo-López, N.; Panizo, S.; Martín-Carro, B.; Mayo Barrallo, J.C.; Román-García, P.; García-Castro, R.; Fernández-Gómez, J.M.; Hevia-Suárez, M.Á.; Martín-Vírgala, J.; Fernández-Villabrille, S.; Martínez-Arias, L.; Vázquez, S.B.; Calleros Basilio, L.; Naves-Díaz, M.; Cannata-Andía, J.B.; Quirós-González, I.; Alonso-Montes, C.; Fernández-Martín, J.L. Redox Metabolism and Vascular Calcification in Chronic Kidney Disease. Biomolecules 2023, 13, 1419.

Abstract

Vascular calcification (VC), is a common complication in patients with chronic kidney disease and increases mortality. Although oxidative stress is involved in the onset and progression of this disorder, the specific role of some main redox regulators such as catalase, the main scavenger of H2O2, remains unclear. In the present study, epigastric arteries of kidney transplant recipients, an in vivo model of VC and an in vitro model of VC exhibiting catalase overexpression (Cts) were analyzed. Peri-calcification areas of human epigastric arteries have increased levels of catalase and cytoplasmic rather than nuclear RUNX2. In the in vivo model, advanced aortic VC concurs with lower levels of the H2O2 scavenger, glutathione peroxidase 3 compared to controls. In an early model of calcification using vascular smooth muscle cells (VSMCs), Cts VSMCs showed the expected increase in RUNX2 total levels. However, Cts VMSC also exhibited lower percentage of the nucleus stained for RUNX2 in response to calcifying media. At this early model of VC we did not observe dysregulation of mitochondrial redox state, an increase in general redox state was observed in the cytoplasm. These in vivo and in vitro results highlight the complex role of antioxidant enzymes as catalase in the process of VC by regulation of RUNX2 location.

Keywords

Vascular calcification; Catalase; CKD; RUNX2; Epigastric arteries; DIGE

Subject

Biology and Life Sciences, Biochemistry and Molecular Biology

Comments (0)

We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.

Leave a public comment
Send a private comment to the author(s)
* All users must log in before leaving a comment
Views 0
Downloads 0
Comments 0
Metrics 0


×
Alerts
Notify me about updates to this article or when a peer-reviewed version is published.
We use cookies on our website to ensure you get the best experience.
Read more about our cookies here.