Key result
Cardiac 12/15-LOX overexpression induced systolic dysfunction and fibrosis via MCP-1-mediated macrophage infiltration, whereas its disruption improved pressure overload-induced heart failure.
Why the study?
Does 12/15-LOX overexpression or disruption affect the development of heart failure and cardiac inflammation in mouse models?
Population
Preclinical models including Dahl salt-sensitive rats, Alox15 transgenic mice, Alox15-deficient mice, and…
Comparison
Genetic overexpression of 12/15-LOX, genetic… vs Wild-type littermates, sham-operated mice, or…
Design
Preclinical
Follow-up
Up to 48 weeks of age or 14 days
Authors
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Suggests 12/15-LOX inhibition as experimental HF target; leaves open human translation and clinical validation.
Does 12/15-LOX overexpression or disruption affect the development of heart failure and cardiac inflammation in mouse models?
Cardiac 12/15-LOX promotes heart failure development through MCP-1-mediated macrophage infiltration, suggesting 12/15-LOX inhibition as a potential therapeutic target.
Kayama et al. (2009) studied Heart failure. 12/15-LOX overexpression or disruption vs. Wild-type mice was evaluated on Systolic dysfunction and cardiac fibrosis. Cardiac 12/15-LOX overexpression induced systolic dysfunction and fibrosis via MCP-1-mediated macrophage infiltration, whereas its disruption improved pressure overload-induced heart failure.
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