Oxidative Medicine and Cellular Longevity最新文献

[This corrects the article DOI: 10.1155/2019/5972575.].

[This retracts the article DOI: 10.1155/2021/3672112.].

[This retracts the article DOI: 10.1155/2017/1206420.].

Background: Oxidative stress plays a crucial role in the pathogenesis of preeclampsia. Given that the NADPH quinone oxidoreductase 1 (NQO1) is an important enzyme in the antioxidant system, this study aimed to investigate the relationship between the NQO1 rs1800566 polymorphism, NQO1 promoter methylation, and oxidative stress with the risk of preeclampsia.

Methods: This case-control study analyzed 170 women, including preeclampsia patients and healthy pregnant women. To investigate the NQO1 rs1800566 variants, the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used. Promoter methylation analysis in 96 of these samples was conducted using quantitative methylation-specific PCR (qMSP) method. Glutathione peroxidase (GPx) and superoxide dismutase (SOD) activity, along with zinc (Zn), copper (Cu), selenium (Se), malondialdehyde (MDA), and total antioxidant capacity (TAC) levels were measured using chemical methods.

Results: We found reduced levels of TAC, Zn, and Se, and also the SOD activity in patients than controls. However, the MDA and Cu levels, and the GPx activity increased in preeclamptic patients. No association was identified between the NQO1 rs1800566 variants or NQO1 promoter methylation with the risk of preeclampsia.

Conclusion: It seems the NQO1 rs1800566 and the promoter methylation of NQO1 gene are not involved in the risk of preeclampsia. However, our findings indicate the presence of oxidative stress in preeclamptic patients.

Obesity-associated metabolic dysfunction is closely linked to chronic low-grade inflammation, or metaflammation, which is predominantly driven by changes in AT homeostasis. Macrophages, key components of the innate immune system, are central regulators of this inflammatory process. In lean AT, resident macrophages (AT-associated macrophages [ATMs]) exhibit an anti-inflammatory phenotype and support tissue homeostasis. However, during obesity, AT undergoes hypoxia, mechanical stress, and lipid overload, leading to immune cell infiltration and a phenotypic switch of ATMs toward a proinflammatory M1 profile. This shift contributes to systemic inflammation and obesity-associated metabolic risks. Here, we review the current understanding of macrophage polarization in obesity, highlighting the transcriptomic plasticity and functional heterogeneity of ATMs, their interactions within the AT microenvironment, and the formation of crown-like structures (CLSs) as a structural hallmark of AT inflammation. We also discuss the regulatory functions of transcription factors, such as hypoxia-inducible factor (HIF) 1α (HIF-1α) and peroxisome proliferator activated receptor gamma (PPARγ), that control the phenotypic switch of macrophages in healthy and obese ATs. Furthermore, we examined emerging macrophage subsets, such as CD9⁺ and Trem2⁺ lipid-associated macrophages (LAMs), and their dual roles in AT remodeling and inflammation. Understanding the complex network of macrophage activation in obese AT is essential for identifying therapeutic targets aimed at mitigating obesity-associated metabolic risk and restoring tissue function.

[This retracts the article DOI: 10.1155/2020/8026838.].

[This retracts the article DOI: 10.1155/2023/6916819.].

[This retracts the article DOI: 10.1155/2018/4501097.].

[This corrects the article DOI: 10.1155/2022/7038834.].

[This corrects the article DOI: 10.1155/2021/2860488.].