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Aldosterone, mitochondria and regulation of cardiovascular metabolic disease.
Tsai, Cheng-Hsuan; Chen, Zheng-Wei; Lee, Bo-Ching; Liao, Che-Wei; Chang, Yi-Yao; Tsai, Yan-Rou; Chou, Chia-Hung; Wu, Vin-Cent; Hung, Chi-Sheng; Lin, Yen-Hung.
Affiliation
  • Tsai CH; Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
  • Chen ZW; National Taiwan University Hospital Primary Aldosteronism Center, Taipei, Taiwan.
  • Lee BC; Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital Yun-Lin Branch, Yun-Lin, Taiwan.
  • Liao CW; Department of Medical Imaging, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
  • Chang YY; Department of Medicine, National Taiwan University Cancer Center, Taipei, Taiwan.
  • Tsai YR; Cardiology Division of Cardiovascular Medical Center, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
  • Chou CH; Division of Cardiology, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
  • Wu VC; Department of Obstetrics and Gynecology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
  • Hung CS; National Taiwan University Hospital Primary Aldosteronism Center, Taipei, Taiwan.
  • Lin YH; Division of Nephrology, Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
J Endocrinol ; 263(1)2024 Oct 01.
Article in En | MEDLINE | ID: mdl-39121045
ABSTRACT
Aldosterone is a mineralocorticoid hormone involved in controlling electrolyte balance, blood pressure, and cellular signaling. It plays a pivotal role in cardiovascular and metabolic physiology. Excess aldosterone activates mineralocorticoid receptors, leading to subsequent inflammatory responses, increased oxidative stress, and tissue remodeling. Various mechanisms have been reported to link aldosterone with cardiovascular and metabolic diseases. However, mitochondria, responsible for energy generation through oxidative phosphorylation, have received less attention regarding their potential role in aldosterone-related pathogenesis. Excess aldosterone leads to mitochondrial dysfunction, and this may play a role in the development of cardiovascular and metabolic diseases. Aldosterone has the potential to affect mitochondrial structure, function, and dynamic processes, such as mitochondrial fusion and fission. In addition, aldosterone has been associated with the suppression of mitochondrial DNA, mitochondria-specific proteins, and ATP production in the myocardium through mineralocorticoid receptor, nicotinamide adenine dinucleotide phosphate oxidase, and reactive oxygen species pathways. In this review, we explore the mechanisms underlying aldosterone-induced cardiovascular and metabolic mitochondrial dysfunction, including mineralocorticoid receptor activation and subsequent inflammatory responses, as well as increased oxidative stress. Furthermore, we review potential therapeutic targets aimed at restoring mitochondrial function in the context of aldosterone-associated pathologies. Understanding these mechanisms is vital, as it offers insights into novel therapeutic strategies to mitigate the impact of aldosterone-induced mitochondrial dysfunction, thereby potentially improving the outcomes of individuals affected by cardiovascular and metabolic disorders.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Cardiovascular Diseases / Aldosterone / Metabolic Diseases / Mitochondria Limits: Animals / Humans Language: En Journal: J Endocrinol Year: 2024 Document type: Article Affiliation country: Taiwan Country of publication: United kingdom

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Cardiovascular Diseases / Aldosterone / Metabolic Diseases / Mitochondria Limits: Animals / Humans Language: En Journal: J Endocrinol Year: 2024 Document type: Article Affiliation country: Taiwan Country of publication: United kingdom