ArticleFundamental research2026
Targeting C3aR/STAT3 signaling attenuates neuroinflammation and reverses neurological impairment in Neuromyelitis optica.
Article in Fundamental research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Abundant evidence indicates that the interaction between astrocytes and microglia through the C3-C3a receptor (C3aR) pathway is a crucial contributor to the pathogenesis of neurodegenerative and autoimmune disorders, such as neuromyelitis optica (NMO). However, the role of C3aR in microglia in modulating inflammation related to local lesions and neurological dysfunctions in NMO remains unclear. In this study, we reveal for the first time that the expression of C3aR on microglia is positively correlated with microglial activation, proinflammatory cytokine secretion, and complement deposition, which results in the typical NMO-like lesion characterized by astrocyte injury with aquaporin 4 (AQP4) loss, demyelination, and motor neuron loss, as well as cognitive impairments, visual defects, and locomotor deficits in different models of NMO. The knockdown of C3aR or the use of a C3aR antagonist, both
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