Cuproptosis-driven astrocyte reactivity exacerbates experimental cerebral malaria pathogenesis.

ABSTRACT:

Background

Cerebral malaria (CM), a lethal neurological complication of Plasmodium falciparum, is characterized by blood-brain barrier (BBB) disruption. Although astrocytes constitute essential components of the BBB neurovascular unit, their immunoregulatory functions during CM pathogenesis remain elusive. Clinical evidence of altered copper homeostasis in patients with CM, coupled with known associations between copper dysregulation and astrocyte reactivity, prompted investigation of cuproptosis-a copper-dependent programmed cell death pathway-in the disease progression of CM.

Methods

Using a P. berghei ANKA (PbA)-induced experimental CM (ECM) model in C57BL/6 mice, we evaluated pharmacological modulation with copper ionophore disulfiram (DSF) versus copper chelator tetrath

SUBMITTER: Hou X 

PROVIDER: S-EPMC12604326 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature