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慢性阻塞性肺疾病(COPD)是全球第三大死亡原因，1 40岁以上的人中有十分之一患有此病.2 虽然澳门第一赌城在线娱乐对慢性阻塞性肺病生物学的理解已经取得了相当大的进展, 近几十年来，慢性阻塞性肺病的治疗进展缓慢.
作为呼吸医学领域的长期领导者, we are bringing inhaled therapy to COPD and leading the science to deliver next generation treatments with the potential to reduce exacerbations, hospitalisations and mortality. We are committed to developing new therapies that target the underlying drivers of COPD to move beyond exacerbation prevention and symptom control to slow and reverse disease progression by enhancing lung regeneration.
Beyond treatment, we are working with governments and policy makers around the world to address systemic challenges and make COPD a public health priority – including Act on COPD, a programme designed to educate and provide resources to change the mindset of COPD care and to reduce hospitalisations and mortality. In a separate initiative, 澳门第一赌城在线娱乐正在合作开展首个COPD质量改善项目, 实现COPD护理卓越标准的质量改进倡议合作(CONQUEST), that aims to improve outcomes for patients at greater risk of future COPD exacerbations by developing and implementing quality standards into routine care and measuring implementation success.
通过在各个方面应对慢性阻塞性肺病, we hope to achieve our bold ambition of cutting the COPD exacerbation rate in half by 2030 and reduce the associated cardiovascular mortality risk.
We have an investigational treatment in Phase 1 clinical trials which may provide a new approach to target fibrotic pathways earlier versus other mechanisms in development for IPF. 澳门第一赌城在线娱乐的豪猪抑制剂已被证明可以抑制Wnt信号传导(细胞维持的重要途径), differentiation and renewal), 它在IPF等疾病中非常活跃. 通过抑制目标信号通路, we hope that the novel treatment may be able to slow or prevent fibrosis in IPF and potentially other types of fibrotic diseases.
减缓或逆转疾病进展的
Slowing and ultimately reversing the progression of COPD is critical to improving the devasting outlook for patients today. We are committed to our work in this area and are investing in treatments and trials that will enable us to demonstrate true disease modification – stopping lung function decline over time and reversing the structural damage caused by the disease.
COPD is biologically complex with multiple disease drivers and our scientific strategy is built on our deep understanding of these pathways and the identification of novel drug targets that we can address with our array of new modalities. Using a precision medicine approach from the onset will mean that patients can be matched with the treatments they are most likely to benefit from, right from the start.
在新的疾病途径中追随科学
目前的治疗方法治疗症状，但不能解决慢性阻塞性肺病细胞损伤的根本原因. We are exploring approaches demonstrating disease modification through lung tissue regeneration in a number of novel inflammatory pathways:
Interleukin 33 (IL-33)
IL-33 is a broad-acting cytokine at the top of the inflammatory cascade that is released by the cells lining the lung following cell damage or stress.
IL-33是治疗多种疾病的一个有吸引力的靶点, including COPD, where it is hoped that inhibition of this inflammatory pathway could have the potential to deliver disease modification by addressing the IL-33-driven inflammation associated with tissue remodelling in the lung.3,4 IL-33在中重度COPD患者中升高，且与加重相关.
Our pre-clinical research has shown that blocking the IL-33 pathway can reduce the build-up of goblet cells and mucus production back to levels seen in healthy cells. 此外，IL-33是临床验证的COPD靶点3,4 with emerging clinical data suggesting that IL-33 blockade can improve lung function and reduce exacerbation risk in COPD.
通过澳门第一赌城在线娱乐的基因组学研究中心(CGR)的倡议, we are gaining a better understanding of the potential of IL-33 as a biomarker in COPD and other chronic diseases.
Myeloperoxidase (MPO)
MPO是一种已知与慢性阻塞性肺病炎症的根本原因有关的酶. 在COPD患者的气道中检测到MPO水平升高, 这两者都引发了疾病的恶化, 以及在疾病稳定状态下对肺部的持续和加速损害.5
澳门第一赌城在线娱乐希望抑制这种炎症途径可以在COPD中实现疾病的改变. In addition, higher circulating MPO levels are associated with an increased risk of adverse cardiovascular (CV) outcomes and excess death from CV-related causes,6 which is important to address since CV diseases are some of the most clinically important comorbidities in COPD.
Forkhead box O4 (FOXO4)
FOXO4是一种参与细胞周期控制的转录因子, cell death and metabolism, 作为p53信号通路的一部分.7 Cells exposed to chronic stress, such as with smoking, 是否会受到损伤，但仍能抵抗细胞死亡和肺部清除——一种被称为衰老的状态.8 当这些细胞继续存活, 它们向周围的细胞释放信号分子，从而促进进一步的损伤, 还有炎症和纤维化, leading to chronic disease.9
We have identified a role for the FOXO4-p53 interaction in promoting cellular senescence in the lung and are exploring approaches to disrupt this pathway that would initiate cell death and removal of damaged cells from the lung. In our early research, 澳门第一赌城在线娱乐发现，靶向这种相互作用创造了一个有利于肺再生的环境, leading to improved lung function, 肺气肿造成的损伤也会减少.
Transforming COPD care
澳门第一赌城在线娱乐追求减缓或逆转COPD疾病进展的目标, we are pushing the boundaries of science to tackle the toughest and most complex unsolved problems by targeting the underlying disease drivers and achieving greater efficacy through new modalities and novel combinations. 从一开始就采用精准医疗方法, 同时利用新工具和新技术加速进展, 意味着澳门第一赌城在线娱乐正在迈向一个COPD疾病改变可能成为现实的世界, 这样这些病人就可以开始过得更好, healthier lives. ——而且没有这种使人衰弱和危及生命的状况.
