SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia (BPD) is a chronic and debilitating disease that can exert serious and overwhelming effects on the physical and mental health of premature infants, predominantly due to intractable short- and long-term complications. Oxidative stress is one of the most predominant causes of BPD. Hyperoxia activates a cascade of hazardous events, including mitochondrial dysfunction, uncontrolled inflammation, reduced autophagy, increased apoptosis, and the induction of fibrosis. These events may involve, to varying degrees, alterations in SIRT1 and its associated targets. In the present review, we describe SIRT1-related signaling pathways and their association with BPD. Our intention is to provide new insights into the molecular mechanisms that regulate BPD and identify potential therapeutic targets for this debilitating condition.

Automated summary

BPD is a chronic and debilitating disease that affects premature infants, mainly due to oxidative stress. High levels of oxygen lead to harmful events like mitochondrial dysfunction, inflammation, reduced autophagy, increased apoptosis, and fibrosis. Understanding the signaling pathways related to SIRT1 could potentially lead to new therapeutic targets for BPD.