Loss of TSPOAP1 exacerbates mitochondrial dysfunction and neuronal apoptosis after intracerebral hemorrhage

Intracerebral hemorrhage (ICH) induces severe secondary neuronal injury, in which mitochondrial dysfunction and apoptosis play central roles. Accumulating evidence suggests that mitochondrial failure represents a critical convergence point linking diverse injurious stimuli to neuronal apoptosis after ICH. However, the molecular mechanisms that connect mitochondrial dysfunction to irreversible apoptotic commitment remain incompletely understood. In particular, the upstream regulators governing mitochondrial permeability transition pore (mPTP) opening during ICH have yet to be fully defined.