SIRT1-Related Signaling Pathways and Their Association With Bronchopulmonary Dysplasia

Kun Yang1, Wenbin Dong1

  • 1Department of Newborn Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, China.

Frontiers in Medicine
|March 11, 2021
PubMed

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.

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