Deficiency in Aim2 affects viability and calcification of vascular smooth muscle cells from murine aortas and angiotensin-II induced aortic aneurysms

• Verfasst von: Wortmann, Markus [VerfasserIn]
• Verfasst von: Hakimi, Maani [VerfasserIn]
• Verfasst von: Böckler, Dittmar [VerfasserIn]
• Verfasst von: Dihlmann, Susanne [VerfasserIn]
• Titel: Deficiency in Aim2 affects viability and calcification of vascular smooth muscle cells from murine aortas and angiotensin-II induced aortic aneurysms
• Verf.angabe: Markus Wortmann, Muhammad Arshad, Maani Hakimi, Dittmar Böckler and Susanne Dihlmann
• E-Jahr: 2020
• Jahr: 15 September 2020
• Umfang: 14 S.
• Fussnoten: Gesehen am 13.11.2020
• Titel Quelle: Enthalten in: Molecular medicine
• Ort Quelle: [London] : BioMed Central, 1994
• Jahr Quelle: 2020
• Band/Heft Quelle: 26(2020,1) Artikel-Nummer 87, 14 Seiten
• ISSN Quelle: 1528-3658
• DOI: doi:10.1186/s10020-020-00212-z
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1738694437
• K10plus-PPN:
  Universitätsbibliothek
• Lokale URL UB: Zum Volltext

Abstract

Phenotypic transformation of vascular smooth muscle cells is a key element in vascular remodeling and aortic aneurysm growth. Previously, deletion of several inflammasome components decreased formation of aortic aneurysm (AA) in the Angiotensin II (AngII) -induced mouse model. We hypothesized that the inflammasome sensor Absent in melanoma 2 (Aim2) might affect the phenotype of vascular smooth muscle cells (VSMC), thereby reducing AA formation.