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Published on: October 31, 2025
SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia
1Department of Newborn Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Insights
Oxidative stress causes bronchopulmonary dysplasia (BPD) in premature infants. This review explores SIRT1 signaling pathways, offering insights into BPD mechanisms and potential therapeutic targets.
Area of Science:
- Neonatal Medicine
- Cellular Biology
- Pulmonary Medicine
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants, often caused by oxidative stress from hyperoxia.
- Hyperoxia triggers mitochondrial dysfunction, inflammation, apoptosis, and fibrosis, contributing to BPD pathogenesis.
- Sirtuin 1 (SIRT1) and its targets are implicated in these detrimental processes.
Purpose of the Study:
- To review SIRT1-related signaling pathways.
- To elucidate the association between SIRT1 and BPD.
- To identify potential therapeutic targets for BPD.
Main Methods:
- Literature review of studies on SIRT1 and BPD.
- Analysis of molecular mechanisms linking oxidative stress, hyperoxia, and BPD.
- Examination of SIRT1's role in cellular events relevant to BPD.
Main Results:
- SIRT1 signaling is significantly altered in the context of hyperoxia-induced lung injury.
- SIRT1 influences key pathways including mitochondrial function, inflammation, autophagy, apoptosis, and fibrosis.
- Specific SIRT1 targets are crucial mediators of BPD development.
Conclusions:
- SIRT1 plays a critical role in the molecular pathogenesis of BPD.
- Understanding SIRT1 pathways offers novel therapeutic strategies for BPD.
- Targeting SIRT1 may mitigate the long-term complications of BPD in premature infants.
Abstract:
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.
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