Key result
Cathepsin L deficiency reduces atherosclerotic lesions and lipid cores in LDLr-knockout mice.
Why the study?
Increased expression of cathepsin L in human atherosclerotic lesions suggests its role in arterial extracellular matrix remodeling and atherogenesis, which was tested in mice.
Does Cathepsin L deficiency reduce diet-induced atherosclerosis in LDLr-knockout mice?
Population
Low-density lipoprotein receptor-deficient mice
Comparison
Cathepsin L deficiency (LDLr-/- Cat L-/-) vs littermate control LDLr-/- Cat L+/- and LDLr-/- Cat L+/+ mice
Design
Preclinical study with genetically modified mice
Follow-up
12 and 26 weeks
Authors
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No practice change indicated; leaves open Cat L inhibition as atherosclerosis therapy in humans.
Does Cathepsin L deficiency reduce diet-induced atherosclerosis in LDLr-knockout mice?
Cathepsin L deficiency reduces diet-induced atherosclerosis in mice, suggesting it plays a direct role in plaque progression and leukocyte transmigration.
Kitamoto et al. (2007) studied Atherosclerosis. Cathepsin L deficiency vs. Littermate control LDLr-/- Cat L+/- and LDLr-/- Cat L+/+ mice was evaluated on Atherosclerotic lesions and lipid cores size. Cathepsin L deficiency in LDLr-knockout mice significantly reduced atherosclerotic lesions, lipid cores, and extracellular matrix degradation after 12 and 26 weeks of a Western diet.
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