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Observational analysis uncovered neuroinflammatory modulation via microglial autophagy after intracerebral hemorrhage, suggesting miR-92a-3p as a therapeutic target.
These findings establish miR-92a-3p as a critical regulator of microglial autophagy and inflammation after hemorrhagic stroke and identify it as a prospective therapeutic target for neuroinflammatory modulation.
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Hao et al. (2025) studied this question.
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