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治疗急性呼吸窘迫综合征的代谢改变。

Therapeutic targeting of metabolic alterations in acute respiratory distress syndrome.

机构信息

Wellcome-Wolfson Institute for Experimental Medicine, Queen's University of Belfast, Belfast, UK.

出版信息

Eur Respir Rev. 2020 Jul 3;29(156). doi: 10.1183/16000617.0114-2020. Print 2020 Jun 30.

Abstract

Acute respiratory distress syndrome (ARDS) remains a significant source of mortality in critically ill patients. Characterised by acute, widespread alveolar inflammation and pulmonary oedema, its pathophysiological heterogeneity has meant that targeted treatments have remained elusive. Metabolomic analysis has made initial steps in characterising the underlying metabolic derangements of ARDS as an indicator of phenotypical class and has identified mitochondrial dysfunction as a potential therapeutic target. Mesenchymal stem cells and their derived extracellular vesicles have shown significant promise as potential therapies in delivering mitochondria in order to redivert metabolism onto physiological pathways.

摘要

急性呼吸窘迫综合征(ARDS)仍然是危重病患者死亡的主要原因。其特征为急性、广泛的肺泡炎症和肺水肿,其病理生理学异质性意味着靶向治疗仍然难以捉摸。代谢组学分析已初步确定 ARDS 的潜在代谢紊乱作为表型分类的指标,并确定线粒体功能障碍是潜在的治疗靶点。间充质干细胞及其衍生的细胞外囊泡作为潜在的治疗方法具有很大的应用前景,它们可以递送线粒体,以使代谢重新转向生理途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b68/9488567/84ee28e8a447/ERR-0114-2020.01.jpg

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