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Aldosterone Excess Induced Mitochondria Decrease and Dysfunction via Mineralocorticoid Receptor and Oxidative Stress

Cheng-Hsuan Tsai1,2,3, Chien-Ting Pan3,4, Yi-Yao Chang1,5

  • 1Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan University, Taipei 100, Taiwan.

Biomedicines
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Aldosterone excess damages cardiac mitochondria, reducing ATP production and DNA. Mineralocorticoid receptor antagonists and antioxidants mitigate these effects, revealing a key pathway in heart disease.

Keywords:
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Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Endocrinology

Background:

  • Aldosterone excess is implicated in cardiac dysfunction and remodeling in conditions like primary aldosteronism and heart failure.
  • The specific impact of aldosterone excess on cardiac mitochondria remains largely uncharacterized.
  • Understanding mitochondrial response is crucial for developing targeted therapies for aldosterone-related heart conditions.

Purpose of the Study:

  • To investigate the effects of aldosterone excess on cardiac mitochondrial function and dysfunction.
  • To elucidate the underlying mechanisms, including signaling pathways and oxidative stress, in both cellular and in vivo models.
  • To evaluate the therapeutic potential of mineralocorticoid receptor antagonists and antioxidants.

Main Methods:

  • Utilized H9c2 cardiomyocytes for in vitro studies to assess mitochondrial DNA, protein expression (COX IV, SOD2), and ATP production.
  • Employed an in vivo aldosterone-infused ICR mice model to mirror clinical conditions.
  • Analyzed the role of the mineralocorticoid receptor (MR)/MAPK/p38/reactive oxygen species (ROS) pathway.

Main Results:

  • Aldosterone excess significantly reduced mitochondrial DNA, COX IV and SOD2 protein levels, and ATP production in H9c2 cells.
  • In vivo, aldosterone infusion led to decreased cardiac mitochondrial DNA and COX IV protein.
  • Both in vitro and in vivo, the detrimental effects of aldosterone were attenuated by MR antagonists and antioxidants, implicating oxidative stress.

Conclusions:

  • Aldosterone excess directly induces mitochondrial dysfunction and loss in cardiac cells.
  • The mineralocorticoid receptor and associated oxidative stress are key mediators of aldosterone-induced cardiac mitochondrial damage.
  • Targeting the MR pathway and oxidative stress presents a promising therapeutic strategy for managing aldosterone-related cardiac pathology.