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In DCM, the upregulation of mitogen-activated protein kinase kinase kinase kinase 4 (MAP4K4) induces S-nitrosylation of Drp1 (SNO-Drp1) and suppresses GPX4 expression, culminating in mitochondrial dysfunction and endothelial cell ferroptosis, which exacerbates cardiac microvascular damage

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Parallel studies indicate that physiologic dopamine signaling generally inhibits NLRP3 activity via receptor-mediated pathways, implying that the gradual loss of dopamine in PD removes an endogenous anti-inflammatory brake, exacerbating neuroinflammation

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