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METTL14 Regulates Adipose Tissue Macrophage Polarization via JAK2/STAT3 Pathway to Attenuate Obstructive Sleep

Yijing Zhang1,2, Ze-Hua Zhao3, Chaojie Li1

  • 1Department of Otorhinolaryngology, Qilu Hospital of Shandong University, NHC Key Laboratory of Otorhinolaryngology (Shandong University), Jinan, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 26, 2026
PubMed

Insights

Obstructive sleep apnea (OSA) involves altered m6A RNA methylation, with METTL14 downregulation exacerbating adipose inflammation. Restoring METTL14 may treat OSA-related metabolic issues and inflammation via the JAK2/STAT3 pathway.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Immunology

Background:

  • Obstructive sleep apnea (OSA) is linked to metabolic dysfunction and systemic inflammation.
  • The specific role of m6A RNA methylation in OSA-related metabolic disturbances remains unclear.
  • Identifying key regulators of m6A methylation in OSA is crucial for understanding disease mechanisms.

Purpose of the Study:

  • To identify the critical m6A RNA methylation regulator involved in OSA-induced adipose tissue inflammation.
  • To investigate the underlying molecular mechanisms by which this regulator impacts OSA.
  • To explore the therapeutic potential of targeting m6A RNA methylation in OSA.

Main Methods:

  • Analysis of m6A methylation regulator expression and association with inflammation markers in OSA patients.
  • Establishment of a mouse model of OSA using high-fat diet and chronic intermittent hypoxia (CIH).
  • In vitro assays to determine the effects of methyltransferase-like 14 (METTL14) on macrophage polarization and JAK2/STAT3 signaling.

Main Results:

  • Global m6A RNA methylation levels and regulator expression were altered in OSA patients.
  • METTL14 expression was negatively associated with systemic inflammation and downregulated in OSA mouse models and hypoxia-treated macrophages.
  • METTL14 overexpression inhibited M1 macrophage polarization and suppressed the JAK2/STAT3 pathway by promoting JAK2 mRNA decay.

Conclusions:

  • METTL14 plays a significant role in regulating adipose tissue dysfunction and metabolic inflammation associated with OSA.
  • Dysregulation of METTL14 contributes to OSA-induced inflammation and metabolic disorders.
  • Targeting m6A RNA methylation of the JAK2/STAT3 pathway presents a potential therapeutic strategy for OSA-related complications.
Keywords:
adipose tissue macrophagechronic intermittent hypoxiamethyltransferase‐like 14obstructive sleep apneasystemic inflammation

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