系统性红斑狼中JAK抑制剂:将病变发生转化为治疗
Gabriela Ceobanu1, Christopher J Edwards1
1NIHR Southampton Clinical Research Facility, University Hospital Southampton, Southampton, UK.
Lupus
|October 9, 2024
概括
简氏激酶 (JAK) 抑制剂在治疗系统性红斑狼 (SLE),一种自身免疫性疾病方面表现有前途. 本综述总结了关于用于管理SLE爆发和慢性炎症的JAK抑制剂的当前临床数据.
科学领域:
- 免疫学 免疫学 免疫学
- 类风湿病学 类风湿病学
- 药理学 药理学是指药理学的学科.
背景情况:
- 系统性红斑狼 (SLE) 是一种复杂的自身免疫性疾病,通过自身抗体和慢性炎症引起多器官损伤.
- 尽管取得了进展,但SLE仍存在未得到满足的治疗需求,这推动了对新型治疗方法的研究.
- 最近批准的贝利马布和阿尼弗罗马布等药物突显了进展,但向疗法仍在不断发展.
研究的目的:
- 审查现有的临床试验和病例报告数据关于SLE治疗中Janus激酶 (JAK) 抑制剂.
- 探索JAK抑制剂作为针对性口服疗法的潜力,用于管理SLE.
- 总结目前关于SLE患者中JAK抑制剂疗效和安全性的证据基础.
主要方法:
- 对SLE的JAK抑制剂的临床试验和病例报告的文献搜索.
- 分析关于疗效,安全性和患者结局的已公布数据.
- 综合发现,以提供SLE中JAK抑制剂的全面概述.
主要成果:
- 多种JAK抑制剂正在针对SLE进行研究,针对关键的炎症途径.
- 从试验和病例报告中获得的早期数据表明,在管理SLE爆发和疾病活动方面,有潜在的益处.
- 雅克抑制剂提供口服向治疗的选择,扩大了SLE的治疗策略.
结论:
- 雅克抑制剂代表了一种有前途的针对性治疗方法,用于系统性红斑狼.
- 进一步的研究和临床试验至关重要,以确定JAK抑制剂在SLE管理中的最终作用.
- 对JAK抑制剂的探索意味着向SLE患者提供个性化和有效的治疗方法的迈进.
相关概念视频
The JAK-STAT Signaling Pathway
8.7K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
8.7K
Antihypertensive Drugs: Direct Renin Inhibitors
505
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
505
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF
117
Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab...
117
Inhibition of Cdk Activity
4.7K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.7K
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
394
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
394
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
490
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
490


