Life sciences · 2025
Inhibition of NSUN6 protects against intermittent hypoxia-induced oxidative stress and inflammatory response in adipose tissue through suppressing macrophage ferroptosis and M1 polarization.
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Wang Xinyu, Gong Linjing, Wei Chang, Zhao Yuean, Ran Longyi, Li Peijun, Gu Wenyu, Wu Xu, Liang Zongan, Wang Xinyuan
Аннотация
AIMS: Accumulating studies have demonstrated obstructive sleep apnea (OSA) is strongly associated with metabolic syndrome (MetS) and inflammatory response in adipose tissue. Chronic intermittent hypoxia (CIH) has been proved leading to M1 macrophage polarization that contributes to adipose tissue inflammation, but the molecular mechanism remains unclear. Epigenetic regulation of RNA has been found playing crucial roles in incremental diseases.
MAIN METHODS: Based on mining the GEO database, we constructed an IH (8 weeks) C57/6 J mice model to investigate the changes and interactions of key gene expression, M1 macrophage infiltration, and inflammatory markers in white adipose tissue. We also used an IH-treated (24 h) RAW 264.7 cells to further explore the mechanisms of hypoxia-induced M1 polarization, oxidative stress, and inflammatory response.
KEY FINDINGS: According to the analysis of datasets, CIH increases the level of NSUN6 in adipose tissue and NSUN6 shows good diagnostic value of OSA. In the mice model, CIH exposure is also demonstrated to increases NSUN6 level and M1 macrophage infiltration in adipose tissue, which can be reversed by ferroptosis inhibitor. Studies show that CIH leads to ferroptosis and M1 macrophage polarization by promoting the expression of NSUN6 in vitro, thus resulting in inflammatory response.
SIGNIFICANCE: Our findings provide a better understanding of the mechanisms of CIH-induced inflammation in adipose tissue. NSUN6 is firstly suggested to participate in macrophages ferroptosis and M1 polarization. Inhibition of NSUN6 in macrophages could protects against CIH-induce oxidative stress and inflammatory response in adipose tissue, thus becoming a potential therapeutic target to OSA-associated MetS.
MAIN METHODS: Based on mining the GEO database, we constructed an IH (8 weeks) C57/6 J mice model to investigate the changes and interactions of key gene expression, M1 macrophage infiltration, and inflammatory markers in white adipose tissue. We also used an IH-treated (24 h) RAW 264.7 cells to further explore the mechanisms of hypoxia-induced M1 polarization, oxidative stress, and inflammatory response.
KEY FINDINGS: According to the analysis of datasets, CIH increases the level of NSUN6 in adipose tissue and NSUN6 shows good diagnostic value of OSA. In the mice model, CIH exposure is also demonstrated to increases NSUN6 level and M1 macrophage infiltration in adipose tissue, which can be reversed by ferroptosis inhibitor. Studies show that CIH leads to ferroptosis and M1 macrophage polarization by promoting the expression of NSUN6 in vitro, thus resulting in inflammatory response.
SIGNIFICANCE: Our findings provide a better understanding of the mechanisms of CIH-induced inflammation in adipose tissue. NSUN6 is firstly suggested to participate in macrophages ferroptosis and M1 polarization. Inhibition of NSUN6 in macrophages could protects against CIH-induce oxidative stress and inflammatory response in adipose tissue, thus becoming a potential therapeutic target to OSA-associated MetS.