E-cigarette exposure augments murine abdominal aortic aneurysm development: role of Chil1

Cardiovasc Res. 2023 May 2;119(3):867-878. doi: 10.1093/cvr/cvac173.

Abstract

Aims: Abdominal aortic aneurysm (AAA) is a common cardiovascular disease with a strong correlation to smoking, although underlying mechanisms have been minimally explored. Electronic cigarettes (e-cigs) have gained recent broad popularity and can deliver nicotine at comparable levels to tobacco cigarettes, but effects on AAA development are unknown.

Methods and results: We evaluated the impact of daily e-cig vaping with nicotine on AAA using two complementary murine models and found that exposure enhanced aneurysm development in both models and genders. E-cigs induced changes in key mediators of AAA development including cytokine chitinase-3-like protein 1 (CHI3L1/Chil1) and its targeting microRNA-24 (miR-24). We show that nicotine triggers inflammatory signalling and reactive oxygen species while modulating miR-24 and CHI3L1/Chil1 in vitro and that Chil1 is crucial to e-cig-augmented aneurysm formation using a knockout model.

Conclusions: In conclusion our work shows increased aneurysm formation along with augmented vascular inflammation in response to e-cig exposure with nicotine. Further, we identify Chil1 as a key mediator in this context. Our data raise concerns regarding the potentially harmful long-term effects of e-cig nicotine vaping.

Keywords: Abdominal aortic aneurysm; Aortic aneurysm; E-cigarette; Nicotine; Vascular inflammation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Aortic Aneurysm, Abdominal* / chemically induced
  • Aortic Aneurysm, Abdominal* / genetics
  • Electronic Nicotine Delivery Systems*
  • Female
  • Male
  • Mice
  • MicroRNAs* / genetics
  • Nicotine / toxicity
  • Smoking

Substances

  • Nicotine
  • MicroRNAs