Abstract / Description of output
atherosclerotic pathology through both systemic and cell-autonomous changes in vascular smooth muscle cells and macrophages, the two main cell types involved in atherogenesis. CMA deficiency promotes dedifferentiation of vascular smooth muscle cells and a pro-inflammatory state in macrophages. Conversely, a genetic mouse model with upregulated CMA shows lower vulnerability to the pro-atherosclerotic challenge. We propose that CMA could be an attractive therapeutic target against cardiovascular diseases.
|Proceedings of the National Academy of Sciences (PNAS)
|Published - 1 Apr 2022