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Cardiovascular Engineering

Cardiovascular Engineering - Poster Session E

S32 - Effect of mPTP Inhibitors on ROS Generation in Procoagulant Platelets

Saturday, October 11, 2025
10:00 AM - 11:00 AM PDT
Location: Exhibit Hall F, G & H

Introduction: : The mitochondrial permeability transition pore (mPTP) is a channel formed on the inner mitochondrial membrane that drives pathology and cell death. When platelets are strongly activated in cardiovascular disease and thrombosis, a sustained influx of calcium and reactive oxygen species (ROS) formation can trigger the opening of the mPTP and further ROS production. Following mPTP opening, platelets expose the lipid phosphatidylserine (PS) on their surface, which creates a negatively charged surface, promoting the coagulation cascade and platelet activation. This is a key feature that distinguishes procoagulant from aggregatory platelets. While moderate amounts of procoagulant platelets are necessary for hemostasis, excessive production leads to pathological thrombosis, including stroke, deep vein thrombosis, and myocardial infarction. Here, we test whether and how novel, small molecule mPTP inhibitors affect ROS generation and procoagulant platelet activity.

Materials and

Methods: : Platelets were prepared from citrate anticoagulated blood obtained from healthy human donors with an OHSU IRB approved protocol for ROS generation assays. A fluorometric ROS assay was used to measure the effect of mPTP inhibitors (e.g., MC63, TR002) on ROS production in resting and procoagulant platelets (4ยด108/ml) from collagen-related peptide (10 mg/ml CRP-XL) and thrombin (1 U/ml) stimulation.

Results, Conclusions, and Discussions:: Fluorescence imaging studies found less ROS-positive signal on procoagulant platelets pretreated with MC63 or TR002 compared to vehicle alone positive controls. Kinetics studies of ROS generation in a fluorescence plate reader assay also followed temporal changes in ROS production in procoagulant platelets treated with TR and MC63. Our results find a potential effect of mPTP inhibition on the generation of ROS in procoagulant
platelet generation. Future research will specify how mPTP inhibitors specifically interfere with ROS generation to modulate procoagulant platelet activity.

Acknowledgements and/or References (Optional): :