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

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 t...

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Bibliographic Details
Main Authors: Wortmann, Markus (Author) , Hakimi, Maani (Author) , Böckler, Dittmar (Author) , Dihlmann, Susanne (Author)
Format: Article (Journal)
Language:English
Published: 15 September 2020
In: Molecular medicine
Year: 2020, Volume: 26, Issue: 1
ISSN:1528-3658
DOI:10.1186/s10020-020-00212-z
Online Access:Verlag, kostenfrei, Volltext: https://doi.org/10.1186/s10020-020-00212-z
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Author Notes:Markus Wortmann, Muhammad Arshad, Maani Hakimi, Dittmar Böckler and Susanne Dihlmann
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Summary: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.
Item Description:Gesehen am 13.11.2020
Physical Description:Online Resource
ISSN:1528-3658
DOI:10.1186/s10020-020-00212-z

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