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| Mitochondrial control of procoagulant platelets in vascular injury and repair Joe Aslan. |
Abstract
Procoagulant platelets provide a phosphatidylserine (PS) surface that accelerates thrombin generation at sites of vascular disruption, a response that is essential for hemostasis but can also amplify tissue injury and drive pathological thrombosis after vascular disease and intervention. A central trigger for the procoagulant switch is mitochondrial control of calcium handling. Sustained cytosolic calcium loading promotes opening of the mitochondrial permeability transition pore (mPTP), mitochondrial depolarization and feed-forward calcium amplification that commits platelets to a PS-high, thrombin-generating phenotype. This presentation will summarize mechanistic and systems-level evidence that mitochondrial gating events define a discrete platelet program that links injury sensing to coagulation output, and discuss how this program may differentially shape outcomes across tissue contexts, including vascular inflammation, remodeling, and device-associated injury. We will also highlight pharmacologic strategies to modulate mPTP-dependent platelet procoagulant signaling with improved selectivity compared with legacy cyclophilin-dependent agents, and outline how pathway-resolved platelet phenotyping (including phosphoproteomic and functional readouts) can be used to identify patient subsets at risk for thrombotic complications while preserving physiologic repair. Together, these concepts position platelet mitochondrial signaling as a tractable node at the intersection of thrombosis, tissue-specific injury, and vascular healing, with implications for safer antithrombotic development and precision management after vascular interventions.
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