Version 1
: Received: 15 July 2024 / Approved: 15 July 2024 / Online: 16 July 2024 (03:51:35 CEST)
How to cite:
Thimm, C.; Adjaye, J. Sodium deficiency diseases: The association with the renin-angiotensin-aldosterone system, aging and inflammation. Preprints2024, 2024071238. https://doi.org/10.20944/preprints202407.1238.v1
Thimm, C.; Adjaye, J. Sodium deficiency diseases: The association with the renin-angiotensin-aldosterone system, aging and inflammation. Preprints 2024, 2024071238. https://doi.org/10.20944/preprints202407.1238.v1
Thimm, C.; Adjaye, J. Sodium deficiency diseases: The association with the renin-angiotensin-aldosterone system, aging and inflammation. Preprints2024, 2024071238. https://doi.org/10.20944/preprints202407.1238.v1
APA Style
Thimm, C., & Adjaye, J. (2024). Sodium deficiency diseases: The association with the renin-angiotensin-aldosterone system, aging and inflammation. Preprints. https://doi.org/10.20944/preprints202407.1238.v1
Chicago/Turabian Style
Thimm, C. and James Adjaye. 2024 "Sodium deficiency diseases: The association with the renin-angiotensin-aldosterone system, aging and inflammation" Preprints. https://doi.org/10.20944/preprints202407.1238.v1
Abstract
Every individual at some point encounters the progressive biological process of aging which is considered one of the major risk factors for common diseases. The main drivers of aging are oxi-dative stress, senescence, and Reactive oxygen species (ROS). The renin-angiotensin-aldosterone system (RAAS) includes several systematic processes for the regulation of blood pressure which is caused by an imbalance of electrolytes. During activation of RAAS, binding of angiotensin II (ANG II) to angiotensin II type I receptor (AGTR1) activates intracellular NADPH oxidase to generate superoxide anions and promote uncoupling of endothelial NO synthase, which in turn decreases NO availability and increases ROS production. Promoting oxidative stress and DNA damage mediated by ANG II is tightly regulated. Individuals with sodium deficiency-associated diseases such as Gitelman syndrome (GS) and Bartter syndrome (BS) show down-regulation of inflammation-related processes and have reduced oxidative stress and ROS. Additionally, the histone deacetylase-Sirtuin-1(SIRT1) has a significant impact on the aging process with reduced activity with age. However, GS/BS patients generally sustain higher levels of SIRT1 activity than aged-matched healthy individuals.
In this review, we highlight the importance of the hallmarks of aging, inflammation, and the RAAS system in GS/BS patients and how this might impact healthy aging. We further propose fu-ture research directions for studying the etiology of GS/BS at the molecular level using pa-tient-derived renal stem cells and induced pluripotent stem cells.
Biology and Life Sciences, Biochemistry and Molecular Biology
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.
