Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target.
Shared mechanisms of multimorbidity in COPD, atherosclerosis and type-2 diabetes: the neutrophil as a potential inflammatory target.
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DOI：
10.1183/16000617.0102-2019
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发表时间：
2020-03-31
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影响因子：
--
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多发性硬化症越来越常见，目前的医疗保健策略并不总是与治疗这种复杂的疾病负担相一致。COPD、2型糖尿病（T2 D）和心血管疾病（尤其是动脉粥样硬化）一起发生的频率高于预期，即使考虑到吸烟、肥胖、缺乏活动和贫困等风险因素。这支持了统一机制的可能性，有助于每种疾病的发病机制或进展。嗜中性粒细胞炎症与COPD有因果关系，并且在动脉粥样硬化和T2 D的发病机制中越来越多地被认识到，可能在疾病之间形成病因学联系。这种联系可能反映了炎症从一个受影响的器官溢出到体循环中，使所有器官暴露于促炎细胞因子增加的环境中。此外，越来越多的证据支持其他过程参与慢性疾病的发病机制，如细胞衰老或细胞表型的变化。本综述探讨了炎症，细胞衰老和细胞过程的当前科学证据，如COPD，T2 D和动脉粥样硬化发病机制中的活性氧产生和表型变化;突出了这些疾病共有的共同机制。我们确定了针对这些领域的新兴治疗方法，但也需要更多的工作来提高我们对多病背景下潜在细胞生物学的理解。在我们的老龄化人口中，多重死亡越来越普遍。将慢性炎症性疾病的研究集中在一起对于实现有效的医疗干预和防止研究变得孤立至关重要http://bit.ly/32l9hXs
Multimorbidity is increasingly common and current healthcare strategies are not always aligned to treat this complex burden of disease. COPD, type-2 diabetes mellitus (T2D) and cardiovascular disease, especially atherosclerosis, occur more frequently together than expected, even when risk factors such as smoking, obesity, inactivity and poverty are considered. This supports the possibility of unifying mechanisms that contribute to the pathogenesis or progression of each condition. Neutrophilic inflammation is causally associated with COPD, and increasingly recognised in the pathogenesis of atherosclerosis and T2D, potentially forming an aetiological link between conditions. This link might reflect an overspill of inflammation from one affected organ into the systemic circulation, exposing all organs to an increased milieu of proinflammatory cytokines. Additionally, increasing evidence supports the involvement of other processes in chronic disease pathogenesis, such as cellular senescence or changes in cellular phenotypes. This review explores the current scientific evidence for inflammation, cellular ageing and cellular processes, such as reactive oxygen species production and phenotypic changes in the pathogenesis of COPD, T2D and atherosclerosis; highlighting common mechanisms shared across these diseases. We identify emerging therapeutic approaches that target these areas, but also where more work is still required to improve our understanding of the underlying cellular biology in a multimorbid disease setting. Multimorbidity is increasingly common in our ageing population. Drawing together research across chronic inflammatory disease is vital to enable effective medical intervention and prevent research becoming siloed http://bit.ly/32l9hXs
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DOI：
10.1136/heartjnl-2016-310897
发表时间：
2017-10
期刊：
Heart (British Cardiac Society)
影响因子：
--
作者：
Brook RD;Anderson JA;Calverley PM;Celli BR;Crim C;Denvir MA;Magder S;Martinez FJ;Rajagopalan S;Vestbo J;Yates J;Newby DE;SUMMIT Investigators
通讯作者：
SUMMIT Investigators
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发表时间：
2016-01
期刊：
Translational research : the journal of laboratory and clinical medicine
影响因子：
--
作者：
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通讯作者：
Adcock IM
影响因子：
5.6
作者：
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通讯作者：
Andreassi MG
影响因子：
18.2
作者：
Dickson RP;Erb-Downward JR;Martinez FJ;Huffnagle GB
通讯作者：
Huffnagle GB
DOI：
10.1073/pnas.92.20.9363
发表时间：
1995-09-26
影响因子：
11.1
作者：
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通讯作者：
CAMPISI, J