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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| Hauptverfasser: | , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
15 September 2020
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| In: |
Molecular medicine
Year: 2020, Jahrgang: 26, Heft: 1 |
| ISSN: | 1528-3658 |
| DOI: | 10.1186/s10020-020-00212-z |
| Online-Zugang: | Verlag, kostenfrei, Volltext: https://doi.org/10.1186/s10020-020-00212-z
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| Verfasserangaben: | Markus Wortmann, Muhammad Arshad, Maani Hakimi, Dittmar Böckler and Susanne Dihlmann |
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| 520 | |a 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. | ||
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