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Doxycycline induces mitochondrial dysfunction in aortic smooth muscle cells.

Carmen Yap1, Shaynah Wanga2, Rob C I Wüst3

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The antibiotic doxycycline, while anti-inflammatory, impairs mitochondrial function in aortic cells, contributing to aneurysm pathology. The drug elamipretide may mitigate these harmful effects on mitochondrial health.

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Area of Science:

  • Vascular Biology
  • Mitochondrial Medicine
  • Pharmacology

Background:

  • Abdominal aortic aneurysm (AAA) growth is linked to inflammation and mitochondrial dysfunction.
  • Doxycycline, an anti-inflammatory antibiotic, was investigated for AAA therapeutic potential.
  • Mitochondrial dysfunction is a key characteristic of clinical AAA disease.

Purpose of the Study:

  • To investigate the hypothesis that doxycycline impairs mitochondrial function in aortic smooth muscle cells (SMCs).
  • To explore the effects of doxycycline on SMC proliferation, phenotype, and mitochondrial health.
  • To assess the potential of elamipretide (SS-31) in mitigating doxycycline-induced mitochondrial dysfunction in aortic SMCs.

Main Methods:

  • Treatment of aortic SMCs with doxycycline.
  • Analysis of mitonuclear imbalance, proliferation, and contractile protein expression.
  • Investigation of krüppel-like factor 4 (KLF4) role.
  • Administration of elamipretide (SS-31) to doxycycline-treated cells.
  • Assessment of mitochondrial gene expression and connectivity.

Main Results:

  • Doxycycline induced mitonuclear imbalance, reduced SMC proliferation, and decreased contractile protein expression.
  • KLF4 expression increased with doxycycline, but KLF4 knockdown did not alter SMC changes.
  • Elamipretide improved mitochondrial gene expression and connectivity but did not rescue SMC contractility markers.
  • Doxycycline causes mitochondrial dysfunction and SMC phenotypic switching, potentially worsening AAA.

Conclusions:

  • Doxycycline exhibits detrimental effects on aortic SMC mitochondrial function and phenotype, counteracting its anti-inflammatory benefits for AAA.
  • Elamipretide can partially ameliorate doxycycline-induced mitochondrial dysfunction in aortic SMCs.
  • Further research into elamipretide is warranted for aneurysm diseases, especially those with underlying mitochondrial dysfunction.