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肾脏疾病中的 Sirtuins:潜在机制和治疗靶点。

Sirtuins in kidney diseases: potential mechanism and therapeutic targets.

机构信息

Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.

China-Japan Friendship Hospital, Institute of Clinical Medical Sciences, Beijing, China.

出版信息

Cell Commun Signal. 2024 Feb 12;22(1):114. doi: 10.1186/s12964-023-01442-4.

DOI:10.1186/s12964-023-01442-4
PMID:38347622
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10860260/
Abstract

Sirtuins, which are NAD-dependent class III histone deacetylases, are involved in various biological processes, including DNA damage repair, immune inflammation, oxidative stress, mitochondrial homeostasis, autophagy, and apoptosis. Sirtuins are essential regulators of cellular function and organismal health. Increasing evidence suggests that the development of age-related diseases, including kidney diseases, is associated with aberrant expression of sirtuins, and that regulation of sirtuins expression and activity can effectively improve kidney function and delay the progression of kidney disease. In this review, we summarise current studies highlighting the role of sirtuins in renal diseases. First, we discuss sirtuin family members and their main mechanisms of action. We then outline the possible roles of sirtuins in various cell types in kidney diseases. Finally, we summarise the compounds that activate or inhibit sirtuin activity and that consequently ameliorate renal diseases. In conclusion, targeted modulation of sirtuins is a potential therapeutic strategy for kidney diseases. Video Abstract.

摘要

Sirtuins 是 NAD 依赖性 III 类组蛋白去乙酰化酶,参与多种生物学过程,包括 DNA 损伤修复、免疫炎症、氧化应激、线粒体稳态、自噬和细胞凋亡。Sirtuins 是细胞功能和机体健康的重要调节因子。越来越多的证据表明,包括肾脏疾病在内的与年龄相关的疾病的发展与 sirtuins 的异常表达有关,调节 sirtuins 的表达和活性可以有效改善肾脏功能并延缓肾脏疾病的进展。在这篇综述中,我们总结了目前强调 sirtuins 在肾脏疾病中作用的研究。首先,我们讨论了 sirtuin 家族成员及其主要作用机制。然后,我们概述了 sirtuins 在肾脏疾病中各种细胞类型中的可能作用。最后,我们总结了激活或抑制 sirtuin 活性从而改善肾脏疾病的化合物。总之,靶向调节 sirtuins 是治疗肾脏疾病的一种有潜力的治疗策略。视频摘要。

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p53 deacetylation alleviates calcium oxalate deposition-induced renal fibrosis by inhibiting ferroptosis.p53 去乙酰化通过抑制铁死亡缓解草酸钙沉积诱导的肾纤维化。
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Zinc defends against Parthanatos and promotes functional recovery after spinal cord injury through SIRT3-mediated anti-oxidative stress and mitophagy.
肾缺血再灌注损伤中的细胞衰老
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Activation of SIRT1 Reduces Renal Tubular Epithelial Cells Fibrosis in Hypoxia Through SIRT1-FoxO1-FoxO3-Autophagy Pathway.SIRT1 的激活通过 SIRT1-FoxO1-FoxO3-自噬途径减轻缺氧条件下肾小管上皮细胞的纤维化。
Adv Biol (Weinh). 2025 Jul;9(7):e2400583. doi: 10.1002/adbi.202400583. Epub 2025 Apr 8.
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J Nat Med. 2025 Mar;79(2):314-327. doi: 10.1007/s11418-024-01863-6. Epub 2025 Jan 3.
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锌通过 SIRT3 介导的抗氧化应激和线粒体自噬来抵抗 Parthanatos 并促进脊髓损伤后的功能恢复。
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