写的:
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death worldwide,1 affecting one in ten people over 40 years old.2 While there has been considerable progress in our understanding of COPD biology, advances in COPD care for this progressive disease have been slow over recent decades.
As a long-standing leader in respiratory medicine, 澳门第一赌城在线娱乐正在为慢性阻塞性肺病带来吸入疗法，并引领科学开发具有减少病情恶化潜力的新一代疗法, 住院和死亡率. 澳门第一赌城在线娱乐致力于开发新的治疗方法，针对COPD的潜在驱动因素，通过增强肺再生，超越恶化预防和症状控制，减缓和逆转疾病进展.
除了治疗, 澳门第一赌城在线娱乐正在与世界各国政府和决策者合作，应对系统性挑战，并使COPD成为公共卫生重点——包括《澳门第一赌城在线娱乐》, 该规划旨在教育和提供资源，以改变COPD护理的观念，减少住院和死亡率. 在一个单独的倡议中, we are collaborating in a first-of-its-kind COPD quality improvement program, Collaboration on Quality improvement initiative for achieving Ex细胞ence in Standards of COPD care (CONQUEST), 旨在通过制定和实施常规护理质量标准并衡量实施成功，改善未来COPD恶化风险更高的患者的预后.
By tackling COPD across all fronts, 澳门第一赌城在线娱乐希望实现到2030年将慢性阻塞性肺病恶化率降低一半并降低相关心血管死亡风险的宏伟目标.
澳门第一赌城在线娱乐在1期临床试验中有一种研究性治疗方法，它可能为IPF提供一种新的靶向纤维化途径的方法，而不是其他正在开发的机制. Our porcupine inhibitor has been shown to suppress Wnt signalling (an important pathway in 细胞 maintenance, 分化与更新), which is known to be highly active in diseases like IPF. By suppressing targeted signalling pathways, 澳门第一赌城在线娱乐希望这种新的治疗方法能够减缓或预防IPF和其他类型的纤维化疾病的纤维化.
Working to slow or reverse disease progression
减缓并最终扭转慢性阻塞性肺病的进展对于改善当今患者的灾难性前景至关重要. 澳门第一赌城在线娱乐致力于这一领域的工作，并投资于治疗和试验，这将使澳门第一赌城在线娱乐能够证明真正的疾病改变——阻止肺功能随着时间的推移而下降，并逆转由疾病引起的结构损伤.
慢性阻塞性肺病具有多种疾病驱动因素的生物学复杂性，澳门第一赌城在线娱乐的科学策略建立在澳门第一赌城在线娱乐对这些途径的深刻理解和澳门第一赌城在线娱乐可以通过一系列新模式解决的新药物靶点的确定之上. 从一开始就使用精准医疗方法将意味着患者可以与他们最有可能受益的治疗相匹配, 打从一开始。.
Following the science in novel disease pathways
Current therapies treat symptoms but do not address the underlying causes of 细胞 damage in COPD. 澳门第一赌城在线娱乐正在探索在一些新的炎症途径中通过肺组织再生来证明疾病改变的方法:
白细胞介素33 (IL-33)
IL-33是一种作用广泛的细胞因子，位于炎症级联反应的顶端，在细胞损伤或应激后由肺内膜细胞释放.
IL-33 is an attractive target in multiple diseases, 包括慢性阻塞性肺病, 希望抑制这种炎症途径可以通过解决与肺组织重塑相关的il -33驱动的炎症来提供疾病修饰的潜力.3,4 Increased IL-33 is seen in moderate-to-severe COPD patients and is correlated 与 increased exacerbations.
澳门第一赌城在线娱乐的临床前研究表明，阻断IL-33通路可以减少杯状细胞的积聚和粘液的产生，使其回到健康细胞的水平. Furthermore, IL-33 is a clinically validated target in COPD3,4 与 新出现的临床数据表明，IL-33阻断可以改善肺功能，降低COPD恶化风险.
Through our Centre for Genomics Research (CGR) initiative, 澳门第一赌城在线娱乐对IL-33作为COPD和其他慢性疾病的生物标志物的潜力有了更好的了解.
髓过氧化酶(MPO)
MPO is an enzyme known to be involved in the root causes of inflammation in COPD. Increased levels of MPO have been detected in the airways of patients 与 COPD, driving both the triggering of exacerbations, as well as continued and accelerated damage of the lung in the stable disease state.5
It is hoped that inhibition of this inflammatory pathway could deliver disease modification in COPD. 除了, 较高的循环MPO水平与心血管(CV)不良结局和心血管相关原因导致的过多死亡风险增加有关,6 由于心血管疾病是慢性阻塞性肺病最重要的临床合并症之一，这一点很重要.
叉头箱O4 (FOXO4)
FOXO4 is a transcription factor involved in 细胞 cycle control, 细胞死亡和新陈代谢, as part of the p53 signalling pathway.7 暴露于慢性压力下的细胞, 比如吸烟, can become damaged yet resistant to 细胞 death and clearance from the lung – a state known as senescence.8 As these 细胞s continue to survive, they release signalling molecules to surrounding 细胞s which promotes further damage, as well as inflammation and fibrosis, 导致慢性疾病.9
澳门第一赌城在线娱乐已经确定了FOXO4-p53相互作用在促进肺部细胞衰老中的作用，并正在探索破坏这一途径的方法，该途径将启动细胞死亡并从肺部移除受损细胞. 在澳门第一赌城在线娱乐早期的研究中, we have found that targeting this interaction creates an environment favourable to lung regeneration, 从而改善肺功能, and a decrease in the damage caused by emphysema.
转变COPD护理
As we pursue our ambition to slow or reverse disease progression in COPD, 澳门第一赌城在线娱乐正在突破科学的界限，以潜在的疾病驱动因素为目标，通过新的模式和新的组合实现更大的疗效，解决最棘手和最复杂的未解决问题. Applying a precision medicine approach from the start, while leveraging new tools and technologies to accelerate progress, means we are moving towards a world where disease modification in COPD could become a reality, so these patients can start to live better, 更健康的生活. - and 与out this debilitating and life-threating condition.
