Psmb8, the proteasome subunit-β type-8, is one of the immunoproteasome catalytic subunits, playing a key role in protein homeostasis, inflammation, and immune response. It is involved in various biological processes, and genetic models such as gene knockout mouse models are valuable for studying its functions [1,2,3].

In a myocardial ischemia/reperfusion (I/R) mouse model, cardiomyocyte-specific Psmb8 overexpression alleviated I/R-mediated cardiac injury and dysfunction by reducing mitochondrial division via downregulating Drp1, while Psmb8 knockout mice showed opposite changes. This indicates Psmb8's cardioprotective role in cardiac I/R damage [1]. In manganese-exposed mice, selective inhibition of Psmb8 mitigated neuroinflammation, reduced microglial activation, and alleviated Mn-induced recognition memory impairments and synapse deficits, suggesting Psmb8's role in microglia-mediated neuroinflammation upon Mn exposure [3].

In conclusion, Psmb8 has diverse functions in different physiological and pathological conditions. Mouse models with Psmb8 knockout or overexpression have revealed its significance in heart and nervous system diseases, highlighting its potential as a therapeutic target for ischemic heart disease and manganese-induced neurological disorders.