Central post-stroke pain frequently arises following thalamic hemorrhage, yet the precise biological pathways driving this debilitating transition from acute injury to chronic discomfort remain poorly defined. Recent research demonstrates that extracellular ATP released during tissue damage activates P2X7 receptors, which subsequently triggers a robust and sustained increase in secreted phosphoprotein 1 (SPP1) expression primarily within reactive microglia. This microglia-derived SPP1 acts through an autocrine integrin β1 (ITGB1) signaling loop to maintain a persistent, chemokine-rich pro-nociceptive environment characterized by heightened neuronal hyperexcitability and mechanical allodynia. Experiments utilizing genetic knockouts, targeted RNA interference, and pharmacological inhibitors reveal that interrupting this SPP1-ITGB1 axis significantly alleviates pain behaviors without compromising baseline sensory functions. Ultimately, these findings identify the purinergic-microglial SPP1-ITGB1 program as a fundamental driver of maladaptive sensory plasticity and establish a promising therapeutic target for treating refractory central post-stroke pain.
References:
Dai R, Wu W, Zhou X, et al. A microglial SPP1-ITGB1 feedback loop sustains thalamic hyperexcitability and post-stroke pain[J]. Neuron, 2026.
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