HDAC1 dysregulation promotes pro-inflammatory microglial activation and aggravates post-stroke neuroinflammation
HDAC1 acts as a key repressor of NF-κB-driven pro-inflammatory microglial activation and neuroinflammation in stroke. Its loss exacerbates inflammatory cascades, immune cell infiltration, and neuronal injury, underscoring HDAC1 as a potential therapeutic target for limiting secondary brain damage after ischaemic stroke.
Authors
- Cheng‐Chun Wu (ORCID: https://orcid.org/0000-0002-7084-9208)
- Yu‐Cheng Ho (ORCID: https://orcid.org/0009-0009-6935-3502)
- Hao‐Kuang Wang (ORCID: https://orcid.org/0000-0002-1928-7502)
- Yung‐Kuo Lee (ORCID: https://orcid.org/0000-0003-1638-8049)
- Jen‐Sue Chen (ORCID: https://orcid.org/0000-0002-5973-8670)
- Tian‐Huei Chu (ORCID: https://orcid.org/0000-0003-1197-5754)
- Yun Lin (ORCID: https://orcid.org/0000-0001-9705-6972)
- Yu-Ting Su
- Cheng-Loong Liang
Institutions
- National Defense University (US)
- National Sun Yat-sen University (TW)
- Chang Gung University (TW)
- Kaohsiung Chang Gung Memorial Hospital (TW)
- Zuoying Armed Forces General Hospital (TW)
- Kaohsiung Armed Forces General Hospital (TW)
- National Defense Medical College (JP)
- National Defense Medical Center (TW)
- I-Shou University (TW)
Publication Details
- Journal
- Annals of Medicine
- Published
- 2025-12-12
- DOI
- https://doi.org/10.1080/07853890.2025.2597624
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00