ER-stress-dependent microparticles derived from smooth muscle cells promote endothelial dysfunction during thoracic aortic aneurysm and dissection

In conclusion, our study demonstrated that elevated mechanical stretch induced MPs formation in SMCs leading to endothelial dysfunction, which is ER stress-dependent. ER stress inhibition suppressed ECs apoptosis, inflammation in aorta and TAAD development.
Source: Clinical Science - Category: Biomedical Science Authors: Tags: PublishAheadOfPrint Source Type: research