Abstract

Cellular senescence is a cell fate implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and chronic obstructive pulmonary disease (COPD). Cellular senescence occurs in response to cellular stressors such as oxidative stress, DNA damage, telomere shortening, and mitochondrial dysfunction. Whether these stresses induce cellular senescence or an alternative cell fate depends on the type and magnitude of cellular stress, but also on intrinsic factors regulating the cellular stress response. Non-coding RNAs, including both microRNAs and long non-coding RNAs, are key regulators of cellular stress responses and susceptibility to cellular senescence. In this review, we will discuss cellular mechanisms that contribute to senescence in IPF and COPD and highlight recent advances in our understanding of how these processes are influenced by non-coding RNAs. We will also discuss the potential therapeutic role for targeting non-coding RNAs to treat these chronic lung diseases.

Highlights

  • Norihito Omote and Maor Sauler*Critical Care and Sleep Medicine Section, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States

  • Chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are chronic lung diseases that disproportionately affect the elderly and impose a significant global health burden

  • NRF2 activity decreases with age and impaired NRF2 activity is implicated in the pathogenesis of IPF and COPD [31, 56,57,58,59]

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Summary

Norihito Omote and Maor Sauler*

Critical Care and Sleep Medicine Section, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, United States. Reviewed by: Marta Bueno, University of Pittsburgh, United States Jonathan Baker, Imperial College London, United Kingdom. Specialty section: This article was submitted to Pulmonary Medicine, a section of the journal

Frontiers in Medicine
INTRODUCTION
In vivo role in fibrosis
Inhibits DNA repair and apoptosis Inhibits DNA damage response
Findings
CONCLUSION
Full Text
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