MicroRNA‐34a Mediates the Aldosterone‐Induced Acceleration of Endothelial Senescence

Inappropriate aldosterone production relative to sodium status is known to induce arterial hypertension and cause detrimental effects on endothelium and vascular remodeling. This study investigated whether microRNAs (miRs) serve as key mediators of aldosterone’s effects on endothelial dysfunction. U...

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Published inInternational journal of hypertension Vol. 2025; no. 1; p. 2339598
Main Authors Jia, Minyue, Lin, Liya, Yang, Boyun, Yu, Hanxiao, Zhong, Shan, Xu, Xiaohong, Song, Xiaoxiao
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.01.2025
Wiley
Subjects
Aldosterone
Apoptosis
Bioinformatics
Cardiovascular disease
Cell cycle
Cell growth
Corticosteroids
Endothelium
Genes
Hypertension
MicroRNA
MicroRNAs
Reagents
Senescence
Telomerase
North Carolina
China
United States > US
Germany
microRNA-34a
NOTCH1
cellular senescence
endothelial dysfunction
aldosterone
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Abstract Inappropriate aldosterone production relative to sodium status is known to induce arterial hypertension and cause detrimental effects on endothelium and vascular remodeling. This study investigated whether microRNAs (miRs) serve as key mediators of aldosterone’s effects on endothelial dysfunction. Using human umbilical vein endothelial cells (HUVECs) as a model system, we demonstrated that aldosterone treatment suppressed cellular proliferation and migration while promoting senescence. Mechanistically, we observed that aldosterone exposure significantly upregulated miR‐34a expression in HUVECs. The functional significance of miR‐34a was confirmed when specific inhibitors reversed aldosterone’s antiproliferative and prosenescence effects. To elucidate the underlying molecular pathway, we performed comprehensive biological analyses, which revealed that miR‐34a target genes were predominantly associated with the Notch signaling pathway. Western blot analysis further validated that miR‐34a promotes senescence in HUVECs through negative regulation of NOTCH1. Collectively, our findings identify miR‐34a as a crucial mediator of aldosterone‐induced endothelial cell senescence via the NOTCH1 signaling pathway, suggesting its potential as a therapeutic target for aldosterone‐related vascular diseases.
AbstractList Inappropriate aldosterone production relative to sodium status is known to induce arterial hypertension and cause detrimental effects on endothelium and vascular remodeling. This study investigated whether microRNAs (miRs) serve as key mediators of aldosterone's effects on endothelial dysfunction. Using human umbilical vein endothelial cells (HUVECs) as a model system, we demonstrated that aldosterone treatment suppressed cellular proliferation and migration while promoting senescence. Mechanistically, we observed that aldosterone exposure significantly upregulated miR-34a expression in HUVECs. The functional significance of miR-34a was confirmed when specific inhibitors reversed aldosterone's antiproliferative and prosenescence effects. To elucidate the underlying molecular pathway, we performed comprehensive biological analyses, which revealed that miR-34a target genes were predominantly associated with the Notch signaling pathway. Western blot analysis further validated that miR-34a promotes senescence in HUVECs through negative regulation of NOTCH1. Collectively, our findings identify miR-34a as a crucial mediator of aldosterone-induced endothelial cell senescence via the NOTCH1 signaling pathway, suggesting its potential as a therapeutic target for aldosterone-related vascular diseases.
Inappropriate aldosterone production relative to sodium status is known to induce arterial hypertension and cause detrimental effects on endothelium and vascular remodeling. This study investigated whether microRNAs (miRs) serve as key mediators of aldosterone's effects on endothelial dysfunction. Using human umbilical vein endothelial cells (HUVECs) as a model system, we demonstrated that aldosterone treatment suppressed cellular proliferation and migration while promoting senescence. Mechanistically, we observed that aldosterone exposure significantly upregulated miR-34a expression in HUVECs. The functional significance of miR-34a was confirmed when specific inhibitors reversed aldosterone's antiproliferative and prosenescence effects. To elucidate the underlying molecular pathway, we performed comprehensive biological analyses, which revealed that miR-34a target genes were predominantly associated with the Notch signaling pathway. Western blot analysis further validated that miR-34a promotes senescence in HUVECs through negative regulation of NOTCH1. Collectively, our findings identify miR-34a as a crucial mediator of aldosterone-induced endothelial cell senescence via the NOTCH1 signaling pathway, suggesting its potential as a therapeutic target for aldosterone-related vascular diseases.Inappropriate aldosterone production relative to sodium status is known to induce arterial hypertension and cause detrimental effects on endothelium and vascular remodeling. This study investigated whether microRNAs (miRs) serve as key mediators of aldosterone's effects on endothelial dysfunction. Using human umbilical vein endothelial cells (HUVECs) as a model system, we demonstrated that aldosterone treatment suppressed cellular proliferation and migration while promoting senescence. Mechanistically, we observed that aldosterone exposure significantly upregulated miR-34a expression in HUVECs. The functional significance of miR-34a was confirmed when specific inhibitors reversed aldosterone's antiproliferative and prosenescence effects. To elucidate the underlying molecular pathway, we performed comprehensive biological analyses, which revealed that miR-34a target genes were predominantly associated with the Notch signaling pathway. Western blot analysis further validated that miR-34a promotes senescence in HUVECs through negative regulation of NOTCH1. Collectively, our findings identify miR-34a as a crucial mediator of aldosterone-induced endothelial cell senescence via the NOTCH1 signaling pathway, suggesting its potential as a therapeutic target for aldosterone-related vascular diseases.
Audience Academic
Author Jia, Minyue
Song, Xiaoxiao
Yang, Boyun
Zhong, Shan
Lin, Liya
Yu, Hanxiao
Xu, Xiaohong
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Copyright Copyright © 2025 Minyue Jia et al. International Journal of Hypertension published by John Wiley & Sons Ltd.
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Copyright © 2025 Minyue Jia et al. International Journal of Hypertension published by John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License (the “License”), which permits use, distribution and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0
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Keywords microRNA-34a
NOTCH1
cellular senescence
endothelial dysfunction
aldosterone
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– ident: e_1_2_14_24_2
  doi: 10.3389/fcvm.2021.784044
– ident: e_1_2_14_38_2
  doi: 10.1111/ggi.13927
– ident: e_1_2_14_21_2
  doi: 10.1155/2017/2872156
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Snippet Inappropriate aldosterone production relative to sodium status is known to induce arterial hypertension and cause detrimental effects on endothelium and...
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StartPage 2339598
SubjectTerms Aldosterone
Apoptosis
Bioinformatics
Cardiovascular disease
Cell cycle
Cell growth
Corticosteroids
Endothelium
Genes
Hypertension
MicroRNA
MicroRNAs
Reagents
Senescence
Telomerase
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Title MicroRNA‐34a Mediates the Aldosterone‐Induced Acceleration of Endothelial Senescence
URI https://www.ncbi.nlm.nih.gov/pubmed/40226530
https://www.proquest.com/docview/3189548906
https://www.proquest.com/docview/3189921858
https://doaj.org/article/96542cbaeeb2453089fff2663ea9bbee
Volume 2025
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