Deficiency of the lysosomal cysteine protease cathepsin L (Ctsl) in mice results in a
phenotype affecting multiple tissues, including thymus, epidermis, and hair follicles, and in
the heart develops as a progressive dilated cardiomyopathy (DCM). To understand the role
of Ctsl in the maintenance of regular heart morphology and function, it is critical to determine
whether the DCM in Ctsl-/-mice is primarily because of the lack of Ctsl expression and
activity in the cardiomyocytes or is caused by the additional extracardiac pathologies …