ArticleJournal of molecular modeling2026
Selective inhibition of platelet inflammatory tether formation via force-modulated vibrational states of integrin αIIbβ3.
Article in Journal of molecular modeling, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
contextPlatelet inflammatory tether (PITT) formation under pathological shear is a central driver of thrombo-inflammation and bleeding complications in severe infections, yet current antiplatelet therapies lack selectivity because they target equilibrium integrin affinity rather than force-dependent adhesion dynamics. The mechanistic origin of catch-bond stabilization in integrin αIIbβ3 under inflammatory shear, and its separation from physiological hemostatic adhesion, therefore remains unresolved.
methodHere, we develop a quantum-informed mechanochemical model that explicitly links shear-induced mechanical loading to the vibrational energy landscape of the metal-ion-dependent adhesion site (MIDAS) of integrin αIIbβ3. Within a Born-Oppenheimer-reduced framework, the MIDAS coordination mode is represented as a force-deformed anharmonic potential, enabling analytic determination of force-dependent vibrational eigenstates, transition-state barriers, and dissociation kinetics. These quantum-derived descriptors are systematically mapped onto stochastic escape and mechanokinetic formalisms to predict bond lifetimes under shear. The model demonstrates that catch-bond behavior emerges from force-induced spectral compression and curvature softening of the MIDAS energy landscape, producing a finite mechanochemical window in which bond lifetime is maximized. We further identify a separation between a kinetic critical force governing lifetime optimization and a higher spectral critical force associated with structural destabilization. This separation provides a physical basis for selectively suppressing PITT formation through modulation of force-sensitive transition-state energetics while preserving low-force hemostatic adhesion. Our results establish energy-landscape engineering as a first-principles strategy for force-selective antiplatelet intervention and a general theoretical framework for mechanosensitive biological adhesion.
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