Work

MiR-92a-3p regulates microglial autophagy and inflammation after intracerebral hemorrhage via ATG14

Year: 2025

Type: article

Abstract: BACKGROUND: Intracerebral hemorrhage (ICH) is a prevalent cerebrovascular event that triggers secondary brain injury in which microglial activation is central. This study explored how miR-92a-3p governs autophagy and inflammatory signaling in this context. METHODS: An in vitro ICH model was established using rat microglia exposed to hemoglobin, with lipopolysaccharide to induce autophagy. Cells were transfected with miR-92a-3p mimics or inhibitors. Apoptosis, miR-92a-3p/ATG14 expression, autophagy-related proteins (LC3, P62), and pro-inflammatory factors were assessed via molecular and cellular assays. RESULTS: Dual luciferase assays and ATG14 silencing confirmed direct targeting of ATG14 by miR-92a-3p. Upregulation of miR-92a-3p suppressed autophagy and thereby reduced inflammatory cytokine release, whereas inhibition of miR-92a-3p restored autophagic activity and reduced inflammation. CONCLUSION: 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.

Source: Neurological Research

DOI: 10.1080/01616412.2025.2594598

Authors: Lin Yao, Qian He, Shengyun Hao, Li Tu, Teng Luo, Qiong Mu

Institutions: Affiliated Hospital of Guizhou Medical University, Tongren Hospital

Language: English

Topic: Intracerebral and Subarachnoid Hemorrhage Research

Subfield: Neurology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Funder: National Natural Science Foundation of China