MYOCD and hypertensive disorder: However, in an AngII-induced hypertension model, AngII promoted Kruppel-like factor 5 (KLF5) expression and KLF5-myocardin binding, disrupted the feedback loop between ANO1 and myocardin, and then antagonised ANO1 transcription in human aortic SMCs, subsequently inducing cellular proliferation and vascular remodelling (51).