带有保护正电荷的抗血栓涂层通过控制XII-生物界面结合因子来防止接触激活
Haifeng Ji1,2, Kai Yu1,2, Srinivas Abbina1,2
1Centre for Blood Research & Life Science Institute, University of British Columbia, Life Sciences Centre, Vancouver, British Columbia, Canada.
Nature materials
|November 12, 2024
概括
这项研究开发了一种新的抗血栓表面,优化了与凝血因子XII的相互作用,以防止血块形成,而不妨碍正常的血液凝结. 这种新的涂层策略为接触血液的设备提供了更好的安全性.
科学领域:
- 生物材料科学 生物材料科学
- 表面化学 表面化学
- 血液静止和血栓形成研究
背景情况:
- 接触血液的医疗器械需要抗血栓表面,以防止器件诱导的血栓形成,并减少抗凝剂相关的出血风险.
- 目前的策略往往侧重于排斥蛋白质的表面,这可能不是普遍有效的.
- 需要先进的材料来控制凝血激活,而不会损害基本的静血功能.
研究的目的:
- 开发一种新的基质独立的抗血栓聚合物涂层.
- 为了优化与凝血因子XII的相互作用,而不是简单地防止其吸附.
- 为了创建一种涂层,可以防止血栓形成,同时保持血液静止.
主要方法:
- 开发一种具有保护正电荷的聚合物涂层,旨在与凝固因子XII进行特定相互作用.
- 使用人类血液进行体外试验,以评估抗血栓性质.
- 在体内使用子动脉-状静脉分流模型进行体内评估,以证明在生理环境中的有效性.
主要成果:
- 形成的涂层与凝血因子XII有着强烈的相互作用.
- 尽管有强烈的相互作用,但涂层诱导了接触途径的最小互动激活,从而启动了凝块形成.
- 在体外和体内研究证实了涂层的抗血栓疗效,与传统的抗蛋白表面策略相矛盾.
结论:
- 通过优化XII因子相互作用,成功开发了一种新的抗血栓聚合物涂层.
- 这种方法挑战了抗血栓应用中排斥蛋白质表面的传统范式.
- 开发的涂层具有显著的潜力,可以提高各种接触血液的医疗器械的安全性和有效性.
相关概念视频
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
1.2K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
1.2K
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
623
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
623
01:20Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
471
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
471
01:16Clot Retraction and Fibrinolysis
4.2K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
4.2K
01:20Extrinsic and Intrinsic Pathways of Hemostasis
5.7K
Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which...
5.7K
01:09Coagulation
4.9K
The coagulation phase is a critical part of the body's process to prevent blood loss following injury to blood vessels. It involves chemical reactions that form a clot to seal the injured area. The clotting process begins shortly after injury, within 15-20 seconds for severe damage and 1-2 minutes for minor injuries.
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
During the coagulation phase, clotting factors, or procoagulants, play a vital role in initiating and progressing the coagulation cascade. This cascade is a series of reactions...
4.9K