Lixia Yue, Yihe Yan

Department of Critical Care Medicine, Shaoxing People’s Hospital, Shaoxing, Zhejiang, 312000, People’s Republic of China

Correspondence: Yihe Yan, Email yyhyyh1110@sina.com

Abstract: Acute respiratory distress syndrome (ARDS) is a severe and life-threatening pulmonary condition characterized by intense inflammation and disrupted oxygen exchange, which can lead to multiorgan failure. Recent findings have established ARDS as a systemic inflammatory disorder involving complex interactions between lung injury, systemic inflammation, and oxidative stress. This review examines the pivotal role of metabolic disturbances in the pathogenesis of ARDS, emphasizing their influence on inflammatory responses and oxidative stress. Common metabolic abnormalities in ARDS patients, including disruptions in carbohydrate, amino acid, and lipid metabolism, contribute significantly to the disease’s severity. These metabolic dysfunctions interplay with systemic inflammation and oxidative stress, further exacerbating lung injury and worsening patient outcomes. By analyzing the regulatory mechanisms of various metabolites implicated in ARDS, we underscore the potential of targeting metabolic pathways as a therapeutic approach. Such interventions could help attenuate inflammation and oxidative stress, presenting a promising strategy for ARDS treatment. Additionally, we review potential drugs that modulate metabolic pathways, providing valuable insights into the etiology of ARDS and potential therapeutic directions. This comprehensive analysis enhances our understanding of ARDS and highlights the importance of metabolic regulation in the development of effective treatment strategies. Key findings from this review demonstrate that metabolic disturbances, particularly those affecting carbohydrate, amino acid, and lipid metabolism, play critical roles in amplifying inflammation and oxidative stress, underscoring the potential of metabolic-targeted therapies to improve patient outcomes.

Keywords: acute respiratory distress syndrome, pathogenesis, lung injury, metabolism, medication