Key result
In mice with macrophage-targeted uPA overexpression, plasminogen was necessary for uPA-induced cardiac fibrosis and macrophage accumulation, and verapamil treatment significantly attenuated both.
Why the study?
Does verapamil or genetic deletion of plasminogen/uPAR reduce cardiac fibrosis and macrophage accumulation in SR-uPA+/o mice?
Does verapamil or genetic deletion of plasminogen/uPAR reduce cardiac fibrosis and macrophage accumulation in SR-uPA+/o mice?
Plasminogen and calcium channels (inhibited by verapamil), but not uPAR, are critical for uPA-induced cardiac macrophage accumulation and fibrosis in a transgenic mouse model.
Answers are grounded in this paper and cite their sources.
Verapamil attenuates uPA-driven fibrosis in mice; leaves open whether plasminogen or calcium-channel targeting reduces cardiac fibrosis in patients.
No abstract yet. The journal hasn't published one we can show.
No takes yet. Share an insight, caveat, or question.
Stempien‐Otero et al. (2006) studied Cardiac fibrosis. Plasminogen deficiency, uPAR deficiency, and verapamil vs. Control/untreated SR-uPA+/o mice was evaluated on Cardiac fibrosis and macrophage accumulation. In mice with macrophage-targeted uPA overexpression, plasminogen was necessary for uPA-induced cardiac fibrosis and macrophage accumulation, and verapamil treatment significantly attenuated both.
Synapse has enriched 10 related papers. Consider them for comparative context: