2. Academic Validation
  3. Sleep Deprivation Induces Gut Damage via Ferroptosis

Sleep Deprivation Induces Gut Damage via Ferroptosis

  • J Pineal Res. 2024 Aug;76(5):e12987. doi: 10.1111/jpi.12987.
Zi-Jian Zheng 1 2 3,  Hai-Yi Zhang 1 2 3,  Ya-Lin Hu 1 2 3,  Yan Li 1 2 3,  Zhi-Hong Wu 1 2 3,  Zhi-Peng Li 1 2 3,  Dong-Rui Chen 1 2 3,  Yang Luo 1 2 3,  Xiao-Jing Zhang 1 2 3,  Cang Li 1 2 3,  Xiao-Yu Wang 1 2 3,  Dan Xu 1 2 3,  Wei Qiu 4,  Hong-Ping Li 5,  Xiao-Ping Liao 1 2 3,  Hao Ren 1 2 3,  Jian Sun 1 2 3
Affiliations

Affiliations

  • 1 State Key Laboratory for Animal Disease Control and Prevention, South China Agricultural University, Guangzhou, China.
  • 2 Guangdong Laboratory for Lingnan Modern Agriculture, National Risk Assessment Laboratory for Antimicrobial Resistance of Animal Original Bacteria, College of Veterinary Medicine, South China Agricultural University, Guangzhou, China.
  • 3 Guangdong Provincial Key Laboratory of Veterinary Pharmaceutics Development and Safety Evaluation, South China Agricultural University, Guangzhou, China.
  • 4 Department of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
  • 5 Shenzhen Children's Hospital, Shenzhen, China.
PMID: 38975671 DOI: 10.1111/jpi.12987
Abstract

Sleep deprivation (SD) has been associated with a plethora of severe pathophysiological syndromes, including gut damage, which recently has been elucidated as an outcome of the accumulation of Reactive Oxygen Species (ROS). However, the spatiotemporal analysis conducted in this study has intriguingly shown that specific events cause harmful damage to the gut, particularly to goblet cells, before the accumulation of lethal ROS. Transcriptomic and metabolomic analyses have identified significant enrichment of metabolites related to Ferroptosis in mice suffering from SD. Further analysis revealed that melatonin could rescue the ferroptotic damage in mice by suppressing lipid peroxidation associated with ALOX15 signaling. ALOX15 knockout protected the mice from the serious damage caused by SD-associated Ferroptosis. These findings suggest that melatonin and Ferroptosis could be targets to prevent devastating gut damage in Animals exposed to SD. To sum up, this study is the first report that proposes a noncanonical modulation in SD-induced gut damage via Ferroptosis with a clearly elucidated mechanism and highlights the active role of melatonin as a potential target to maximally sustain the state during SD.

Keywords

ER stress; colon; ferroptosis; goblet cells; melatonin; sleep deprivation.

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