Does cathepsin A inhibition attenuate myocardial infarction-induced heart failure on the functional and proteomic levels?
Our proteomic and functional data suggest that cathepsin A inhibition has cardioprotective properties and support a beneficial effect of cathepsin A inhibition in the treatment of heart failure after myocardial infarction.
Thrombocytopenia in HLB219 mice is caused by a recessive mutation in Mpl that abrogates mitogen-activated protein kinase-extracellular signal regulated kinase and janus kinase-signal transducers and activators of transcription signaling.