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Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
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Obstructive Sleep Apnea-induced Endothelial Dysfunction Is Mediated by miR-210.

Fenqing Shang1,2, Shen-Chih Wang3,4, Brendoan Gongol5

  • 1Translational Medicine Centre, Xi'an Chest Hospital, and.

American Journal of Respiratory and Critical Care Medicine
|October 3, 2022
PubMed
Summary

Obstructive sleep apnea (OSA) causes endothelial cell dysfunction via a pathway involving SREBP2 and miR-210, leading to mitochondrial damage. This discovery offers new therapeutic targets for OSA-related cardiovascular disease.

Keywords:
endotheliummiR-210mitochondrial dysfunctionobstructive sleep apnea

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Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Sleep Medicine

Background:

  • Obstructive sleep apnea (OSA) is linked to endothelial cell (EC) dysfunction and cardiovascular issues.
  • The precise mechanisms behind OSA-induced EC impairment remain largely unknown.

Purpose of the Study:

  • To elucidate the mechanism of EC dysfunction caused by OSA.
  • To explore potential therapeutic strategies for OSA-accelerated cardiovascular disease.

Main Methods:

  • Utilized data mining, bioinformatics, EC functional assays, OSA mouse models, and human subject assessments.
  • Analyzed microRNA sequencing, RNA sequencing, and serum miR-210 levels in OSA patients and controls.

Main Results:

  • Identified microRNA 210 (miR-210) as significantly upregulated by intermittent hypoxia in ECs and elevated in OSA patients.
  • Demonstrated that miR-210 and OSA serum impair mitochondrial function in ECs, reducing oxygen consumption and membrane potential.
  • Uncovered a mechanism where SREBP2 activates miR-210, inhibiting iron-sulfur cluster assembly and causing mitochondrial dysfunction; betulin mitigated hypertension in an OSA mouse model.

Conclusions:

  • Established a novel SREBP2-miR-210-mitochondrial dysfunction axis linking OSA to EC dysfunction.
  • This pathway provides new insights into OSA's cardiovascular impact and suggests potential therapeutic targets.