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Endothelial miR-34a deletion guards against aneurysm development despite endothelial dysfunction.

Aleksandra Kopacz1, Damian Kloska1, Anna Bar2

  • 1Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.

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Summary

MicroRNA-34a (miR-34a) drives endothelial cell aging and abdominal aortic aneurysm (AAA) development by regulating NRF2. Inhibiting miR-34a protects against AAA, suggesting therapeutic potential.

Keywords:
Abdominal aortic aneurysmEndothelial cellsEndothelial dysfunctionNRF2miR-34a

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Area of Science:

  • Vascular Biology
  • Molecular Biology
  • Aging Research

Background:

  • Endothelial cell (EC) aging and abdominal aortic aneurysm (AAA) are linked to the transcription factor NRF2.
  • MicroRNA-34a (miR-34a) is a known marker of aging.

Purpose of the Study:

  • To investigate the relationship between miR-34a, NRF2, and vascular function in AAA formation.
  • To elucidate the role of miR-34a in mediating NRF2-dependent EC aging and AAA pathogenesis.

Main Methods:

  • Utilized a mouse model of angiotensin II (Ang II)-induced hypertension and AAA.
  • Investigated miR-34a expression in ECs and serum.
  • Assessed EC function and AAA development in miR-34a knockout mice, including on an NRF2 knockout background.
  • Examined the effect of rapamycin on EC proliferation and identified miR-34a targets (MTA2, SIRT1).

Main Results:

  • Premature NRF2-dependent EC aging is mediated by miR-34a.
  • Ang II infusion increased miR-34a in aortic ECs and serum, correlating with AAA development.
  • Mice lacking endothelial miR-34a were protected from AAA despite severe EC dysfunction, even on an NRF2 KO background.
  • Rapamycin reversed the protective effect of miR-34a deficiency by suppressing Ang II-induced EC proliferation.
  • MTA2, not SIRT1, was identified as a miR-34a target inhibiting Ang II-stimulated EC proliferation.

Conclusions:

  • miR-34a plays a critical role in promoting EC aging and AAA formation.
  • Targeting miR-34a or modulating EC proliferation presents a potential therapeutic strategy for aneurysms.