DDIT3 and inflammatory response: For example, CHOP deficiency alleviated myocardial reperfusion injury by inhibiting myocardial apoptosis and inflammation,15 while ablation of CHOP increased the acute phase mortality in mice with myocardial infarction.16 CHOP-deficient mice were reported to be resistant to lung inflammation and injury induced by lipopolysaccharide (LPS) infusion,12 whereas CHOP deficiency resulted in elevated LPS-induced inflammation and kidney injury.14 However, whether CHOP-mediated ER stress is involved in Ang II-induced cardiac injury is unknown and the role of ER stress in this process remains unclear.