Key result
PAI-1 knockout mice exhibited deregulated expression of profibrotic genes including Ankrd1, Pi16, Egr1, and Timp1 in the heart compared to wildtype hearts and knockout kidneys, driving cardiac-selective fibrosis.
Population
Aged plasminogen activator inhibitor-1 (PAI-1) knockout mice and wildtype mice (hearts and kidneys)
Comparison
PAI-1 knockout vs Wildtype mice and unaffected organs
Design
Preclinical
Authors
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Suggests PAI-1 protects against cardiac fibrosis in mice; leaves open human relevance and clinical translation.
PAI-1 knockout leads to deregulation of specific profibrotic genes in the heart, providing a molecular basis for cardiac-selective fibrosis.
Ghosh et al. (2013) studied Cardiac-selective fibrosis (n=12). PAI-1 knockout vs. Wild-type was evaluated on Differential gene expression profiling. PAI-1 knockout mice exhibited deregulated expression of profibrotic genes including Ankrd1, Pi16, Egr1, and Timp1 in the heart compared to wildtype hearts and knockout kidneys, driving cardiac-selective fibrosis.
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