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Updated: Mar 15, 2026
Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
Published on: June 3, 2016
Effect of chronic intermittent hypoxia on apoptosis based on microbiome-based co-metabolomics
Tingyuan Zeng1, Cheng Niu1, Jianqin Cheng2
1Guizhou University Medical College, Guiyang 550025, Guizhou Province, China.
Background:
Obstructive sleep apnea (OSA) is linked to metabolic dysfunction, but the role of chronic intermittent hypoxia (CIH)-induced mitochondrial apoptosis remains unclear. This study investigated whether CIH-induced lung apoptosis involves gut microbiota and metabolite changes.
Methods:
Mice exposed to CIH were analyzed using 16S rRNA sequencing and GC-MS metabolomics. Apoptosis markers (Drp1, BAX, Bcl-2, Caspase-3) were assessed via Western blot, immunohistochemistry, TUNEL, and electron microscopy.
Results:
(1) CIH disrupted fatty acid metabolism (e.g., decreased arachidonic acid, increased nervonic acid), reversible with Mdivi-1 (mitochondrial fission inhibitor). (2) CIH altered gut microbiota, partially restored by Mdivi-1. (3) KEGG analysis revealed apoptosis, autophagy, and P53 pathway changes. (4) CIH reduced mouse weight and cognitive performance; Mdivi-1 improved these. (5) CIH increased BAX/Caspase-3 and decreased Bcl-2, worsening mitochondrial damage-exacerbated by CCCP (apoptosis inducer) but mitigated by Mdivi-1.
Conclusions:
Mdivi-1 alleviated CIH-induced gut dysbiosis, apoptosis, and mitochondrial damage, while CCCP worsened these effects. Gut microbiota and metabolic changes may mediate CIH-induced lung apoptosis.
