Oxidative stress in acute pancreatitis induced acute lung injury: mechanisms and therapeutic advances

Acute pancreatitis (AP) is a common acute abdominal condition. The trigger of acute lung injury (ALI) is a critical factor affecting unfavorable patient outcomes. Evidence indicates that the mechanisms underlying AP-ALI involve a complex bidirectional interaction between oxidative stress and inflammatory processes. Specifically, the overproduction of reactive oxygen species (ROS), combined with impairment of the antioxidant defense system, is a key aspect of AP-ALI pathophysiology. These biochemical changes, in turn, promote the secretion of inflammatory mediators through the activation of key signaling pathways, such as NF-κB and MAPK, which ultimately lead to damage to lung tissue. Additionally, this process involves changes at the molecular level, including mitochondrial dysfunction, endoplasmic reticulum stress, and programmed cell death. Although preclinical studies in animal models suggest that antioxidant therapy may offer protective effects, applying such treatments in clinical settings faces significant hurdles, including pharmacokinetic issues and side effects. This article provides a comprehensive review of the role of oxidative stress in the development and progression of AP-ALI, examining the potential for creating innovative therapies based on these mechanisms.