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沉默调节蛋白及其在妊娠期糖尿病生理病理学中的意义。

Sirtuins and Their Implications in the Physiopathology of Gestational Diabetes Mellitus.

作者信息

Zgutka Katarzyna, Tkacz Marta, Grabowska Marta, Mikołajek-Bedner Wioletta, Tarnowski Maciej

机构信息

Department of Physiology in Health Sciences, Faculty of Health Sciences, Pomeranian Medical University, 70-210 Szczecin, Poland.

Department of Histology and Developmental Biology, Faculty of Health Sciences, Pomeranian Medical University, 71-210 Szczecin, Poland.

出版信息

Pharmaceuticals (Basel). 2025 Jan 1;18(1):41. doi: 10.3390/ph18010041.

DOI:10.3390/ph18010041
PMID:39861104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11768332/
Abstract

Gestational diabetes mellitus (GDM) imposes serious short- and long-term health problems for the mother and her child. An effective therapeutic that can reduce the incidence of GDM and improve long-term outcomes is a major research priority and is very important for public health. Unfortunately, despite numerous studies, the molecular mechanisms underlying GDM are not fully defined and require further study. Chronic low-grade inflammation, oxidative stress, and insulin resistance are central features of pregnancies complicated by GDM. There is evidence of the involvement of sirtuins, which are NAD+-dependent histone deacetylases, in energy metabolism and inflammation. Taking these facts into consideration, the role of sirtuins in the pathomechanism of GDM will be discussed.

摘要

妊娠期糖尿病(GDM)会给母亲及其孩子带来严重的短期和长期健康问题。一种能够降低GDM发病率并改善长期预后的有效治疗方法是一项重要的研究重点,对公共卫生非常重要。不幸的是,尽管进行了大量研究,GDM潜在的分子机制仍未完全明确,需要进一步研究。慢性低度炎症、氧化应激和胰岛素抵抗是并发GDM的妊娠的主要特征。有证据表明,作为NAD+依赖的组蛋白脱乙酰酶的沉默调节蛋白参与了能量代谢和炎症过程。考虑到这些事实,将讨论沉默调节蛋白在GDM发病机制中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c5/11768332/4cff005a2217/pharmaceuticals-18-00041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c5/11768332/4cff005a2217/pharmaceuticals-18-00041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/36c5/11768332/4cff005a2217/pharmaceuticals-18-00041-g001.jpg

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Rev Assoc Med Bras (1992). 2024 Aug 16;70(8):e20240314. doi: 10.1590/1806-9282.20240314. eCollection 2024.
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Metformin improves cognitive dysfunction through SIRT1/NLRP3 pathway-mediated neuroinflammation in db/db mice.
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