ArticleBiomolecules2026
Heme Oxygenase-1 Contributes to Dampening Proinflammatory Activation in the Human Microglial Cell Line HMC3 and Controls the Transcription Factor IRF5.
Article in Biomolecules, 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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10 authors.
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Abstract
Neuroinflammation is recognized as a pivotal factor in promoting neurodegeneration. However, the molecular mechanisms underlying the dysregulation of proinflammatory signaling in microglial cells remain largely elusive. A prominent role has been ascribed to the TLR4 receptor and its downstream targets, among which the transcription factor IRF5 has recently gained attention. Furthermore, the enzyme HO-1 is known to play a crucial role in mediating an anti-inflammatory phenotype in microglia. This study aims to investigate whether IRF5 is a target of the anti-inflammatory activity of HO-1. Using the human microglial cell line HMC3 and validating the results in RAW264.7 macrophage-like cells, via RT-qPCR, Western blotting, and immunofluorescence, we demonstrated that HO-1 contributes to the resolution of LPS-induced proinflammatory activation. Notably, cell exposure to a pharmacological inhibitor of HO-1 increases IRF5 mRNA expression, while treatment with Hemin, able to increase HO-1 expression, significantly reduces IRF5 phosphorylation. This work suggests a possible crosstalk between HO-1 and IRF5, proposing new druggable molecular targets to counteract neuroinflammation.
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