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LncRNA SNHG1 Knockdown Ameliorates HIV-1 gp120V3 Loop-Induced Microglial Neuroinflammation by Regulating the
Xueqin Yan1, Qin Zuo1, Xinyi Li1
1Department of Pathophysiology, Key Laboratory of the State Administration of Traditional Chinese Medicine, School of Medicine, Jinan University, Guangzhou, Guangdong Province, 510632, China.
Inflammation
|January 5, 2026
Summary
Knocking down lncRNA SNHG1 reduces neuroinflammation in HIV-1-associated neurocognitive disorders (HAND) by enhancing autophagy. This suggests SNHG1 as a potential therapeutic target for HAND.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- HIV-1-associated neurocognitive disorders (HAND) involve chronic central nervous system (CNS) inflammation.
- HIV-1 gp120 protein impairs autophagy, leading to neuroinflammation and cognitive deficits.
Purpose of the Study:
- To investigate the role of lncRNA SNHG1 in HIV-1 gp120-induced microglial inflammation.
- To explore the potential of targeting lncRNA SNHG1 for HAND treatment.
Main Methods:
- Examined lncRNA SNHG1 expression in HIV-1 gp120-stimulated microglia.
- Assessed the impact of SNHG1 knockdown on autophagy markers (ULK1, p62, LC3B II/I ratio) and inflammation.
- Investigated the involvement of the Sirt1-Wnt pathway using specific inhibitors (FH535, EX527).
Main Results:
- lncRNA SNHG1 was upregulated in HIV-1 gp120-induced microglial inflammation.
- SNHG1 knockdown alleviated inflammation by promoting autophagy (increased ULK1, decreased p62, enhanced LC3B II/I ratio).
- SNHG1 knockdown's effects were modulated by autophagy inhibitors and involved the Sirt1-Wnt pathway.
Conclusions:
- lncRNA SNHG1 knockdown enhances autophagy and reduces neuroinflammation, potentially via the Sirt1-Wnt pathway.
- Targeting lncRNA SNHG1 represents a novel therapeutic strategy for HAND.
