Nature Communications Study Reveals Angiotensin-II-Driven Mechanism for Exacerbated Intracerebral Hemorrhage
Cloud-Clone ELISA kits and monoclonal antibody deliver critical tools for unraveling receptor-independent coagulation dysregulation A new study by Nature Communications has revealed a previously unknown receptor-independent mechanism for exacerbating hypertension-related intracerebral hemorrhage (ICH). Angiotensin-II (Ang II) directly binds antithrombin (AT) and triggers heparin-like allosteric activation, disturbing coagulation homeostasis and amplifying cerebral hemorrhage damage. The study also found that higher Ang II levels encourage vascular damage and platelet activation, while simultaneously increasing bleeding susceptibility. The research team hypothesized that Ang II could directly interact with AT, trigger heparan-like anticoagulant activity, disrupt hemostasis and expand hematoma volumes following cerebral vessel rupture. The findings support future rational drug-molecule design.
Publié : il y a 4 heures par SuKi Duan dans Health Science
HUSTON, TX, UNITED STATES, October 26, 2026 /EINPresswire.com/ -- Hypertensive intracerebral hemorrhage (ICH) carries high mortality and disability risks. Researchers have long observed a puzzling “th... [9754 symbols]
