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Thoracic aortic aneurysm/dissection ( TAAD ) is characterized by excessive smooth muscle cell ( SMC ) loss, extracellular matrix ( ECM ) degradation and inflammation. In response to certain stimuli, endoplasmic reticulum ( ER ) stress is activated and regulates apoptosis and inflammation. Excessive apoptosis promotes aortic inflammation and degeneration, leading to  TAAD . Therefore, we studied the role of  ER  stress in  TAAD  formation. A lysyl oxidase inhibitor, 3‐aminopropionitrile fumarate ( BAPN ), was administrated to induce  TAAD  formation in mice, which showed significant  SMC  loss (α‐ SMA  level). Excessive apoptosis ( TUNEL  staining) and  ER  stress ( ATF4  and  CHOP ), along with inflammation, were present in  TAAD  samples from both mouse and human. Transcriptional profiling of  SMCs  after mechanical stress demonstrated the expression of genes for  ER  stress and inflammation. To explore the causal role of  ER  stress in initiating degenerative signalling events and  TAAD , we treated wild‐type (  CHOP   +/+ ) or   CHOP   −/−  mice with  BAPN  and found that   CHOP   deficiency protected against  TAAD  formation and rupture, as well as reduction in α‐ SMA  level. Both  SMC  apoptosis and inflammation were significantly reduced in   CHOP   −/−  mice. Moreover,  SMCs  isolated from   CHOP   −/−  mice were resistant to mechanical stress‐induced apoptosis .  Taken together, our results demonstrated that mechanical stress‐induced  ER  stress promotes  SMCs  apoptosis, inflammation and degeneration, providing insight into  TAAD  formation and progression. © 2015 Authors. Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.

Mechanical stretch‐induced endoplasmic reticulum stress, apoptosis and inflammation contribute to thoracic aortic aneurysm and dissection