Key result
Cathepsin S deficiency exacerbated Angiotensin II-induced cardiac fibrosis and inflammation in mice due to abnormal accumulation of autophagosomes and increased reactive oxygen species in macrophages.
Why the study?
Does Cathepsin S deficiency enhance Ang II-induced cardiac inflammation and fibrosis in mice?
Population
Male Cat S-knockout (Cat S-/-) and littermate wild-type (WT) C57BL/6J mice (n=8 per group)
Comparison
Angiotensin II continuous infusion for 7 days vs Saline continuous infusion for 7 days
Design
Preclinical, Blinded analysis for histology and imaging
Follow-up
7 days
Authors
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Cathepsin S may protect against Ang II-induced cardiac fibrosis in mice; hypothesis-generating and requires human validation before any clinical consideration.
Does Cathepsin S deficiency enhance Ang II-induced cardiac inflammation and fibrosis in mice?
p-value: p=<0.01
Cathepsin S deficiency exacerbates Ang II-induced cardiac inflammation and fibrosis by impairing mitophagy and increasing ROS production in macrophages.
Pan et al. (2012) studied Hypertensive heart disease and cardiac fibrosis (n=32). Cathepsin S deficiency vs. Wild-type (normal Cathepsin S) was evaluated on Cardiac fibrosis area and inflammatory cytokine expression (p=<0.01). Cathepsin S deficiency exacerbated Angiotensin II-induced cardiac fibrosis and inflammation in mice due to abnormal accumulation of autophagosomes and increased reactive oxygen species in macrophages.
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