Key result
PAI-1 deficiency in mice reduced hypertensive glomerulosclerosis but profoundly enhanced hypertension-induced cardiac fibrosis and macrophage infiltration.
Why the study?
Does the plasminogen-plasmin system affect angiotensin II-mediated hypertensive kidney and heart injury in mice?
Population
Mice lacking PAI-1, mice lacking tPa, and wild-type mice
Comparison
Angiotensin II infusion via osmotic mini-pumps… vs Normotensive mice of the respective genotype
Design
Preclinical
Follow-up
4 weeks
Authors
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PAI-1 inhibition may protect kidneys yet exacerbate cardiac fibrosis in hypertension; leaves open net therapeutic utility pending human studies.
Does the plasminogen-plasmin system affect angiotensin II-mediated hypertensive kidney and heart injury in mice?
The plasminogen-plasmin system has a complex, organ-specific role in hypertensive target organ damage, with PAI-1 deficiency protecting the kidney but exacerbating cardiac fibrosis.
Knier et al. (2011) studied Hypertensive kidney and heart injury. PAI-1 and tPa deficiency vs. Wild-type mice and normotensive controls was evaluated on Blood pressure, albuminuria, and tissue fibrosis. PAI-1 deficiency in mice reduced hypertensive glomerulosclerosis but profoundly enhanced hypertension-induced cardiac fibrosis and macrophage infiltration.
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