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烟酰胺腺嘌呤二核苷酸(NAD)、缺氧和芳香烃受体细胞信号在慢性肾脏病中的复杂性。

The complexity of nicotinamide adenine dinucleotide (NAD), hypoxic, and aryl hydrocarbon receptor cell signaling in chronic kidney disease.

机构信息

National Heart Lung and Blood Institute, NIH, BG 10 RM 2C135, 10 Center Drive, Bethesda, MD, 20814, USA.

Kidney Disease Section, NIDDK, NIH, Bethesda, MD, USA.

出版信息

J Transl Med. 2023 Oct 9;21(1):706. doi: 10.1186/s12967-023-04584-8.

Abstract

Early-stage detection of chronic kidney diseases (CKD) is important to treatment that may slow and occasionally halt CKD progression. CKD of diverse etiologies share similar histologic patterns of glomerulosclerosis, tubular atrophy, and interstitial fibrosis. Macro-vascular disease and micro-vascular disease promote tissue ischemia, contributing to injury. Tissue ischemia promotes hypoxia, and this in turn activates the hypoxia-inducible transcription factors (HIFs). HIF-1α and HIF-2α, share a dimer partner, HIF-1β, with the aryl hydrocarbon receptor (AHR) and are each activated in CKD and associated with kidney cellular nicotinamide adenine dinucleotide (NAD) depletion. The Preiss-Handler, salvage, and de novo pathways regulate NAD biosynthesis and gap-junctions regulate NAD cellular retention. In the Preiss-Handler pathway, niacin forms NAD. Niacin also exhibits crosstalk with HIF and AHR cell signals in the regulation of insulin sensitivity, which is a complication in CKD. Dysregulated enzyme activity in the NAD de novo pathway increases the levels of circulating tryptophan metabolites that activate AHR, resulting in poly-ADP ribose polymerase activation, thrombosis, endothelial dysfunction, and immunosuppression. Therapeutically, metabolites from the NAD salvage pathway increase NAD production and subsequent sirtuin deacetylase activity, resulting in reduced activation of retinoic acid-inducible gene I, p53, NF-κB and SMAD2 but increased activation of FOXO1, PGC-1α, and DNA methyltransferase-1. These post-translational responses may also be initiated through non-coding RNAs (ncRNAs), which are additionally altered in CKD. Nanoparticles traverse biological systems and can penetrate almost all tissues as disease biomarkers and drug delivery carriers. Targeted delivery of non-coding RNAs or NAD metabolites with nanoparticles may enable the development of more effective diagnostics and therapies to treat CKD.

摘要

早期发现慢性肾脏病(CKD)对于治疗至关重要,因为治疗可能会减缓甚至有时会阻止 CKD 的进展。不同病因的 CKD 具有相似的肾小球硬化、肾小管萎缩和间质纤维化的组织学模式。大血管疾病和微血管疾病促进组织缺血,导致损伤。组织缺血会导致缺氧,而这反过来又会激活缺氧诱导转录因子(HIFs)。HIF-1α 和 HIF-2α 与芳香烃受体(AHR)共享一个二聚体伴侣 HIF-1β,在 CKD 中被激活,并与肾脏细胞烟酰胺腺嘌呤二核苷酸(NAD)耗竭有关。Preiss-Handler、补救和从头途径调节 NAD 生物合成,缝隙连接调节 NAD 细胞保留。在 Preiss-Handler 途径中,烟酸形成 NAD。烟酸还表现出与 HIF 和 AHR 细胞信号的串扰,调节胰岛素敏感性,这是 CKD 的一种并发症。NAD 从头途径中酶活性的失调会增加循环色氨酸代谢物的水平,这些代谢物会激活 AHR,导致多聚 ADP 核糖聚合酶激活、血栓形成、内皮功能障碍和免疫抑制。在治疗方面,NAD 补救途径的代谢产物可增加 NAD 的产生和随后的 Sirtuin 脱乙酰酶活性,从而减少维甲酸诱导基因 I、p53、NF-κB 和 SMAD2 的激活,但增加 FOXO1、PGC-1α 和 DNA 甲基转移酶-1 的激活。这些翻译后反应也可能通过非编码 RNA(ncRNAs)启动,CKD 中这些 RNA 也会发生改变。纳米颗粒穿越生物系统,几乎可以穿透所有组织,作为疾病生物标志物和药物递送载体。利用纳米颗粒靶向递送非编码 RNA 或 NAD 代谢物,可能会开发出更有效的诊断和治疗 CKD 的方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a0c1/10563221/ae40f920d146/12967_2023_4584_Fig1_HTML.jpg

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