Journal
BIOMEDICINES
Volume 10, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines10051119
Keywords
aldosterone; primary aldosteronism; endothelial cell mitochondria; mitochondrial oxidative stress
Categories
Funding
- Ministry of Science and Technology [MOST 109-2314-B-002 -247 -MY3, 110-2811-B-002 -627, 110-2314-B-002 -134 -MY3, 110-2314-B-002 -237, 107-2314-B-002-264-MY3, 108-2811-B-002-634, 109-2811-B-002-541, 110-2314-B-002-134-MY3, 110-2811-B-002-627]
- National Taiwan University Hospital [NTUH 110-A141, 109-S4673, 110-S5120, UN110-045]
- National Taiwan University Hsin-Chu Hospital [109-HCH023, 110-HCH018]
- National Taiwan University Cancer Center [NTUCCS-111-13]
- Taoyuan General Hospital, Ministry of Health and Welfare [PTH109012, PTH110035, PTH111016]
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Excessive aldosterone suppressed endothelial mitochondria through the MR/mitochondrial ROS pathway, leading to endothelial dysfunction, vascular inflammation, and vascular fibrosis.
Excessive aldosterone secretion causes endothelial dysfunction, vascular inflammation, and vascular fibrosis in patients with primary aldosteronism (PA). Endothelial function is closely related to endothelial mitochondria. However, the effects of elevated aldosterone levels on endothelial mitochondria remain unclear. In this study, we used primary cultured human umbilical vein endothelial cells (HUVECs) to investigate the effects of aldosterone on endothelial mitochondria. Mineralocorticoid receptor (MR) small interfering (si)RNA or glucocorticoid receptor (GR) siRNA were used to confirm the pathway by which aldosterone exerts its effects on the mitochondria of HUVECs. The results showed that excess aldosterone suppressed mitochondrial DNA copy numbers, anti-mitochondrial protein, and SOD2 protein expression in a dose- and time-dependent manner. These effects were attenuated by treatment with MR siRNA, but not with GR siRNA. Furthermore, it was attenuated by treatment with a mitochondria-targeted antioxidant (Mito-TEMPO, associated with mitochondrial reactive oxygen species (ROS) production), but not N-acetyl-L-cysteine (associated with cytosolic ROS production), which suggests that the process was through the mitochondrial ROS pathway, but not the cytosolic ROS pathway. In conclusion, aldosterone excess suppressed endothelial mitochondria through the MR/mitochondrial ROS pathway.
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