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对器官特异性IgA肾病全身机制的不断演变的认识:聚焦于肠-肾相互作用。

The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk.

作者信息

Wang Xin, Zhou Xu-Jie, Qiao Xue, Falchi Mario, Liu Jing, Zhang Hong

机构信息

Renal Division, Peking University First Hospital, Beijing, China.

Peking University Institute of Nephrology, Beijing, China.

出版信息

Theranostics. 2025 Jan 1;15(2):656-681. doi: 10.7150/thno.104631. eCollection 2025.

DOI:10.7150/thno.104631
PMID:39744688
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11671385/
Abstract

The interplay between multiple organs, known as inter-organ crosstalk, represents a complex and essential research domain in understanding the mechanisms and therapies for kidney diseases. The kidneys not only interact pathologically with many other organs but also communicate with other systems through various signaling pathways. It is of paramount importance to comprehend these mechanisms for the development of more efficient therapeutic strategies. Despite extensive research in IgA nephropathy (IgAN), the most common kidney disease, the elaboration mechanism of IgAN remains challenging. Numerous studies suggest that alterations in the intestinal microbiome and its metabolites are pivotal in the progression of IgAN, opening new avenues for understanding its mechanisms. Interestingly, certain presumed probiotics, such as , have been implicated in the onset of IgAN, making the exploration of gut microbiota in the context of IgAN pathogenesis even more intriguing. In this review, we summarize the status of gut microbiology studies of IgAN and explore the possible mechanisms and intervention prospects. Future research and treatment directions may increasingly emphasize systemic, multi-organ combined interventions to decelerate the advancement of kidney disease and enhance the overall prognosis of patients.

摘要

多个器官之间的相互作用,即器官间串扰,是理解肾脏疾病机制和治疗方法的一个复杂且重要的研究领域。肾脏不仅在病理上与许多其他器官相互作用,还通过各种信号通路与其他系统进行交流。理解这些机制对于开发更有效的治疗策略至关重要。尽管对最常见的肾脏疾病——IgA肾病(IgAN)进行了广泛研究,但IgAN的发病机制仍具有挑战性。大量研究表明,肠道微生物群及其代谢产物的改变在IgAN的进展中起关键作用,为理解其机制开辟了新途径。有趣的是,某些假定的益生菌,如……,已被认为与IgAN的发病有关,这使得在IgAN发病机制背景下探索肠道微生物群变得更加引人入胜。在本综述中,我们总结了IgAN肠道微生物学研究的现状,并探讨了可能的机制和干预前景。未来的研究和治疗方向可能会越来越强调系统性、多器官联合干预,以减缓肾脏疾病的进展,提高患者的整体预后。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/c6f330b398e1/thnov15p0656g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/d5a4857c817c/thnov15p0656g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/f0ce1cef0cbb/thnov15p0656g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/cfc45ced728b/thnov15p0656g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/c6f330b398e1/thnov15p0656g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/d5a4857c817c/thnov15p0656g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/f0ce1cef0cbb/thnov15p0656g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/cfc45ced728b/thnov15p0656g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ea7/11671385/c6f330b398e1/thnov15p0656g004.jpg

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本文引用的文献

1
Morphine-induced intestinal microbial dysbiosis drives TLR-dependent IgA targeting of gram-positive bacteria and upregulation of CD11b and TLR2 on a sub-population of IgA B cells.吗啡诱导的肠道微生物失调导致 TLR 依赖性 IgA 靶向革兰氏阳性菌,并上调 IgA B 细胞亚群上的 CD11b 和 TLR2。
Gut Microbes. 2024 Jan-Dec;16(1):2417729. doi: 10.1080/19490976.2024.2417729. Epub 2024 Oct 23.
2
Safety and efficacy assessment of fecal microbiota transplantation as an adjunctive treatment for IgA nephropathy: an exploratory clinical trial.粪便微生物群移植作为IgA肾病辅助治疗的安全性和疗效评估:一项探索性临床试验
Sci Rep. 2024 Oct 2;14(1):22935. doi: 10.1038/s41598-024-74171-4.
3
Causal relationship between dietary intake and IgA nephropathy: a Mendelian randomization study.
饮食摄入与IgA肾病之间的因果关系:一项孟德尔随机化研究。
Front Nutr. 2024 Sep 2;11:1400907. doi: 10.3389/fnut.2024.1400907. eCollection 2024.
4
Gut and respiratory microbiota landscapes in IgA nephropathy: a cross-sectional study.IgA 肾病的肠道和呼吸道微生物组景观:一项横断面研究。
Ren Fail. 2024 Dec;46(2):2399749. doi: 10.1080/0886022X.2024.2399749. Epub 2024 Sep 9.
5
Fecal let-7b and miR-21 directly modulate the intestinal microbiota, driving chronic inflammation.粪便 let-7b 和 miR-21 直接调节肠道微生物群,从而引发慢性炎症。
Gut Microbes. 2024 Jan-Dec;16(1):2394249. doi: 10.1080/19490976.2024.2394249. Epub 2024 Sep 3.
6
Gut Microbiota Dysbiosis, Oxidative Stress, Inflammation, and Epigenetic Alterations in Metabolic Diseases.代谢性疾病中的肠道微生物群失调、氧化应激、炎症和表观遗传改变
Antioxidants (Basel). 2024 Aug 14;13(8):985. doi: 10.3390/antiox13080985.
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Microbiota-gut-brain axis: interplay between microbiota, barrier function and lymphatic system.微生物群-肠-脑轴:微生物群、屏障功能和淋巴系统之间的相互作用。
Gut Microbes. 2024 Jan-Dec;16(1):2387800. doi: 10.1080/19490976.2024.2387800. Epub 2024 Aug 25.
8
B-Cell Epigenetic Modulation of IgA Response by 5-Azacytidine and IgA Nephropathy.5-氮杂胞苷对B细胞IgA应答的表观遗传调控与IgA肾病
J Am Soc Nephrol. 2024 Dec 1;35(12):1686-1701. doi: 10.1681/ASN.0000000000000441. Epub 2024 Aug 13.
9
Humoral immune responses primed by the alteration of gut microbiota were associated with galactose-deficient IgA1 production in IgA nephropathy.肠道微生物群改变引发的体液免疫应答与 IgA 肾病中半乳糖缺乏 IgA1 的产生有关。
Front Immunol. 2024 Jul 22;15:1415026. doi: 10.3389/fimmu.2024.1415026. eCollection 2024.
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Targeting Lactobacillus johnsonii to reverse chronic kidney disease.靶向约翰逊乳杆菌以逆转慢性肾脏病。
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