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The Role Of Oxidative Stress As A Mechanism In The Pathogenesis Of Heart Failure In Acute Kidney Injury
Version 1
: Received: 21 May 2024 / Approved: 22 May 2024 / Online: 22 May 2024 (09:47:57 CEST)
How to cite: Tasic, D. The Role Of Oxidative Stress As A Mechanism In The Pathogenesis Of Heart Failure In Acute Kidney Injury. Preprints 2024, 2024051418. https://doi.org/10.20944/preprints202405.1418.v1 Tasic, D. The Role Of Oxidative Stress As A Mechanism In The Pathogenesis Of Heart Failure In Acute Kidney Injury. Preprints 2024, 2024051418. https://doi.org/10.20944/preprints202405.1418.v1
Abstract
Despite a large amount of research on synchronous and mutually induced kidney and heart damage, the basis of the disease is still not fully clarified. Healthy mitochondria are essential for normal kidney and heart function. Mitochondrial dysfunction occurs when the clearance or process of generation and fragmentation of mitochondria is disturbed. The kidney is the second organ after the heart in the number of mitochondria. Kidney tubules are rich in mitochondria due to the high energy requirements for absorption processes of large amounts of ultrafiltrate and dissolved substances.
The place of action of oxidative stress is the influence on the balance in the production and breakdown of mitochondrial reactive oxygen species .
A more precise determination of the place and role of key factors that play a role in the onset of the disease is necessary for understanding the nature of the onset of the disease and the creation of therapy in the future.
The narrative review integrates results found in previously performed studies which have evaluated oxidative stress participation in renocardial syndrome type 3.
Keywords
oxidative stress; acute heart failure; cardiorenal syndrome
Subject
Medicine and Pharmacology, Medicine and Pharmacology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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