Terazosin Attenuates Neuronal Pyroptosis by Regulating the Mitochondrial ROS/NLRP3 Inflammasome Axis Through Mitophagy in Cerebral Ischemia–Reperfusion Injury
Wei Wang, Xin‐Yue Han, Li‐An Huang, Yu‐Sheng Zhang, Heng Meng, An‐Ding Xu · 2026
Read Terazosin Attenuates Neuronal Pyroptosis by Regulating the Mitochondrial ROS/NLRP3 Inflammasome Axis Through Mitophagy in Cerebral Ischemia–Reperfusion Injury by Wei Wang, Xin‐Yue Han, Li‐An Huang, Yu‐Sheng Zhang, Heng Meng, An‐Ding Xu (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/pmc-13399670.txt.
Description
Wang and co-authors test, in 2026, whether the blood pressure drug terazosin can protect brain neurons after stroke reperfusion, when blood returning to the brain deepens injury. In a mouse model of cerebral ischemia-reperfusion and in HT-22 nerve cells starved of oxygen and glucose, injury showed neuronal pyroptosis, inflammatory cell death. It came alongside reactive oxygen species and a fired-up NLRP3 inflammasome, with mitophagy, the disposal of mitochondria, suppressed.
Terazosin reversed this in a dose-dependent manner. It restored mitophagy markers such as LC3B and Beclin-1, cut reactive oxygen buildup, and quieted the NLRP3 inflammasome. That reduced the death proteins and interleukins IL-1-beta and IL-18 that pyroptosis releases. Infarct volume shrank and nerve function improved in the treated mice. Blocking mitophagy with Mdivi-1 or forcing inflammasome activation with nigericin weakened the drug's protection, tying its benefit to the mitophagy-ROS-NLRP3 axis the authors propose.
Catalog record
| CREATOR | Wei Wang, Xin‐Yue Han, Li‐An Huang, Yu‐Sheng Zhang, Heng Meng, An‐Ding Xu |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 47 KB |
| VERSION | 1.0 |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |