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Related Experiment Video

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March2 Alleviates Aortic Aneurysm/Dissection by Regulating PKM2 Polymerization.

Yiran E Li1,2,3,4,5, Shuolin Liu1,2,6,3,4,5, Litao Wang1,2,3,4,5

  • 1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases (Y.E.L., S.L., Litao Wang, Y.D., L. Wu, H.C., T.Z., J.L., S.X., L.L., J.G., J.R., Y.Z.), Zhongshan Hospital, Fudan University, China.

Circulation Research
|March 13, 2025
PubMed
Summary

March2 acts as a protective factor against aortic aneurysm and dissection (AAD) by preventing vascular smooth muscle cell apoptosis. Targeting March2 could offer a new therapeutic strategy for treating AAD.

Keywords:
aminopropionitrileaortic aneurysmaortic dissectioncardiovascular diseasesubiquitin

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Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Genetics

Background:

  • Aortic aneurysm/dissection (AAD) is a critical cardiovascular condition with limited pharmacological treatments.
  • Protein ubiquitination is implicated in cardiovascular diseases, but the role of E3 ubiquitin ligase March2 in AAD is not well understood.

Purpose of the Study:

  • To investigate the role of March2 in the pathogenesis of AAD.
  • To explore March2's mechanism in regulating vascular smooth muscle cell apoptosis and its potential as a therapeutic target.

Main Methods:

  • Integrated single-cell RNA sequencing on human AAD tissues.
  • Generation of smooth muscle cell-specific March2 knockout mouse models.
  • Induction of AAD using β-aminopropionitrile monofumarate and assessment of March2's role.
  • Analysis of histone H3K18 lactylation targets using CUT&Tag-qPCR.

Main Results:

  • March2 expression is reduced in human and mouse AAD models.
  • March2 deficiency exacerbates AAD, while its restoration rescues the pathology.
  • March2 interacts with PKM2, influencing K33-linked polyubiquitination and mitigating AAD-induced histone H3K18 lactylation.
  • PKM2 activation alleviates March2 deficiency-induced AAD severity.

Conclusions:

  • March2 functions as an endogenous protective factor against AAD by inhibiting vascular smooth muscle cell apoptosis.
  • March2 emerges as a promising therapeutic target for the treatment of aortic aneurysm and dissection.