Ученые выявили белок SERPINB3, который делает тромбы устойчивыми к лечению инсульта

The Protein That Hardens Blood Clots The discovery of SERPINB3 opens a new line of research into why some blood clots are more resistant to stroke therapies. DDuring an ischemic stroke, every minute counts. When a clot blocks a cerebral artery, the priority is to restore blood flow as quickly as possible to prevent further tissue death. Mechanical thrombectomy a procedure in which a device is guided to the blocked vessel to remove the clot has radically changed the treatment of the most severe cases. But there is a paradox that neurology is still trying to solve: opening the artery does not always mean the brain receives enough blood again. A study published in June 2026 in the journal Blood provides a new piece of that puzzle. Scientists from Jinan University and other institutions in China identified a protein called SERPINB3 that appears to play an important role in the formation and hardening of clots associated with ischemic stroke. When a Blood Clot Becomes a More Resistant Obstacle The finding begins with an observation that may seem paradoxical: a thrombus is not simply a passive mass blocking an artery. It is a complex biological structure made up of blood cells, proteins, fibrin, collagen and immune cells. Among the latter, researchers found a particularly significant presence of neutrophils, cells that normally help defend the body against infection. By analyzing clots removed from patients using three-dimensional imaging and spatial proteomics, the team found that SERPINB3 was particularly enriched in neutrophils within the thrombi. Its presence was associated with greater amounts of collagen, increased clot stiffness and worse clinical outcomes. The proposed explanation is particularly important. Researchers found that SERPINB3 produced by neutrophils activates a molecular pathway involving transforming growth factor beta 1 (TGF-β1), along with neutrophil extracellular traps (NETs) and COL1A1, a protein associated with collagen production. The result is a thrombus that can become progressively more compact and resistant. Opening the Artery Is Not Always Enough Here lies one of the major challenges in modern stroke medicine. Thrombectomy can restore blood flow through a large cerebral artery, but smaller vessels and the microcirculation may remain compromised. Residual or microscopic clots and inflammation can contribute to the so-called “no-reflow” phenomenon, in which blood fails to circulate adequately through brain tissue even though the main artery appears to be open. That is why roughly half of patients treated with thrombectomy do not achieve complete functional independence at 90 days in various series and reviews, even when successful reperfusion is achieved. The problem is no longer simply removing the clot; it is also understanding what happens in the tissue and blood vessels afterward. The new study points directly toward that territory. In experimental models, reducing SERPINB3 delayed vascular obstruction, improved the effectiveness of treatments designed to dissolve clots and was associated with better neurological recovery. A Potential New Path, Still Far From Patients The discovery is promising, but it does not yet represent an available treatment for people experiencing a stroke. A substantial portion of the evidence comes from animal models and relatively small analyses of human samples: 19 thrombi were used to link clot architecture with collagen and stiffness, while the proteomic analysis included 34 patients and was subsequently validated in another cohort of 22. That means SERPINB3 should, for now, be viewed as a potential therapeutic target, not as a clinically proven solution. But the significance of the finding lies elsewhere: it shifts the focus from the simple act of removing a clot toward the biology that determines why some thrombi are particularly difficult to treat. If future research can safely block this molecular pathway, physicians may one day have a strategy that complements thrombectomy by making certain clots more susceptible to dissolution and potentially improving brain recovery. The question is no longer simply how to remove the clot, but how to prevent its own biology from turning it into an increasingly resistant obstacle.