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Journal of The American Society of Nephrology最新文献

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Clustered Mitochondrial Homolog Inhibition by Lipocalin-2 Orchestrates Mitochondrial Disruption and Contributes to Kidney Disease. 脂钙素-2抑制CLUH介导线粒体破坏并导致肾脏疾病
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-19 DOI: 10.1681/ASN.0000000961
Eloïse Marques, Maraiza Alves Teixeira, Corentin Ramauge Parra, Pierre Isnard, Mairead Kelly-Aubert, Clément Nguyen, Jennifer Lake, Ivan Nemazanyy, Elena I Rugarli, Fabiola Terzi, Morgan Gallazzini
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引用次数: 0
Funding FAIRly: A New Model for Biomedical Research. 公平资助:生物医学研究的新模式。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-17 DOI: 10.1681/ASN.0000001003
Anupam Agarwal, Kurt Marek, Nancy C Andrews, Diego R Vazquez, James Incalcaterra, Ming Lei, Howard Fox, Penny Gordon-Larsen, Jennifer K Lodge, Nick Wigginton, Kelvin Droegemeier
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引用次数: 0
Structural Plasticity of Aged Podocytes Revealed by Volume Electron Microscopy. 体积电镜观察老年足细胞的结构可塑性。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-17 DOI: 10.1681/ASN.0000000979
Takashi Amari, Takayuki Miyaki, Mami Kishi, Jingyuan Xu, Makoto Sugiura, Hisako Kaneda, Yuta Sakai, Rhianna Imura, Yuri Takeuchi, Juan Alejandro Oliva Trejo, Yuto Kawasaki, Takuya Omotehara, Takako Negishi-Koga, Muneaki Ishijima, Junji Yamaguchi, Soichiro Kakuta, Koichiro Ichimura
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引用次数: 0
Authors' Reply: Conceptual and Methodological Considerations in Assessing Disparities after Preemptive Kidney Transplant Waitlisting. 作者回复:评估先发肾移植候补名单后差异的概念和方法考虑。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-16 DOI: 10.1681/ASN.0000000974
Simeon Adeyemo, Deidra C Crews, Krista L Lentine, Fawaz Al Ammary
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引用次数: 0
The Aging Kidney and Acute Kidney Injury. 肾老化与急性肾损伤。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-16 DOI: 10.1681/ASN.0000001002
Karl A Nath, Raman Deep Singh, Anthony J Croatt, Luis A Juncos

Aging is unavoidable and driven, at least in part, by the biologic process termed senescence. Senescence is characterized by cell cycle arrest incurred by one or more stressors wherein there is cellular upregulation of cyclin-dependent kinase inhibitors, p16 Ink4a and/or p21 Cip1 . Senescent cells are metabolically active and resistant to apoptosis, have increased β -galactosidase activity, and express a senescence-associated secretory phenotype (SASP). The SASP produces an array of inflammatory, cytotoxic, fibrotic, and vasoactive factors. Senescence is a diffusible process as, largely through the SASP, a focus of senescent cells can recruit adjacent cells and cells in distant organs, thereby expanding its scope way beyond its original focus. Senescence predisposes not only to chronic diseases (including CKD) but also acute processes (including AKI). This review provides evidence that age increases the risk of human AKI and summarizes clinical factors that predispose older individuals to AKI. It provides an overview of the biology of senescence, and it discusses the role of intrarenal senescent cells in the pathogenesis of AKI, the significance of the extrarenal milieu and distant organs in predisposing to AKI with age, heme as a prosenescent species, and the role of senescence in the AKI to CKD transition. The risk for AKI with aging, in large part, reflects the fact that virtually all processes implicated in AKI, irrespective of age, occur as the kidney ages. Processes discussed include senescent cells, vascular responses, diabetes, impaired NAD + content, sirtuin expression, mitochondrial dysfunction, impaired autophagy, epigenetic changes, telomere shortening, impaired nephroprotectant expression, inflammaging, and immunosenescence. The review concludes by discussing the basis for senolytics (agents that kill senescent cells), senomorphics (agents that block SASP factors), and other aspects of senotherapies.

摘要:衰老是不可避免的,并且至少在一定程度上是由称为衰老的生物过程驱动的。衰老的特征是由一个或多个应激源引起的细胞周期阻滞,其中细胞周期蛋白依赖性激酶抑制剂p16Ink4a和/或p21Cip1上调。衰老细胞代谢活跃,抗凋亡,β-半乳糖苷酶活性增加,并表达衰老相关分泌表型(SASP);SASP产生一系列炎症、细胞毒性、纤维化和血管活性因子。衰老是一个可扩散的过程,主要是通过SASP,衰老细胞的焦点可以招募邻近细胞和远处器官的细胞,从而扩大其范围,远远超出其原始焦点。衰老不仅容易导致慢性疾病(包括CKD),也容易导致急性疾病(包括AKI)。这篇综述提供了年龄增加人类AKI风险的证据,并总结了老年人易患AKI的临床因素。它提供了衰老生物学的概述,并讨论了肾内衰老细胞在AKI发病机制中的作用;肾外环境和远端脏器在老年AKI易感性中的意义;血红素作为一个前衰老种;以及衰老在AKI向CKD过渡中的作用。随着年龄的增长,AKI的风险在很大程度上反映了一个事实,即几乎所有与AKI相关的过程,无论年龄大小,都随着肾脏的衰老而发生。讨论的过程包括衰老细胞、血管反应、糖尿病、NAD+含量受损、sirtuin表达、线粒体功能障碍、自噬受损、表观遗传改变、端粒缩短、肾保护因子表达受损、炎症和免疫衰老。本文最后讨论了抗衰老药物(杀死衰老细胞的药物)、抗衰老药物(阻断SASP因子的药物)和衰老治疗的其他方面的基础。
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引用次数: 0
Glis3 Is a Modifier of Cyst Progression in Autosomal Dominant Polycystic Kidney Disease. Glis3是常染色体显性多囊肾病囊肿进展的修饰因子
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-16 DOI: 10.1681/ASN.0000000980
Zemeng Wei, Jianlei Gu, Xin Tian, Chao Zhang, Hongyu Zhao, Stefan Somlo
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引用次数: 0
Conceptual and Methodological Considerations in Assessing Disparities after Preemptive Kidney Transplant Waitlisting. 评估先发肾移植候补名单后差异的概念和方法考虑。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-16 DOI: 10.1681/ASN.0000000973
Gu Chen, Zhen Wang
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引用次数: 0
CFHR3*B Haplotype, Complement Activation, and Risk of IgA Nephropathy. CFHR3*B单倍型、补体激活与IgA肾病的风险
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-15 DOI: 10.1681/ASN.0000000983
Yongji Zhang, Honghong Zou, Xinran Ni, Fenghong Tie, Boyang Xu, Yuqi Kang, Weiyi Xiang, Yaxin Li, Changhao Jia, Ying Tan, Lijun Liu, Jicheng Lv, Junyu Xiao, Gaosi Xu, Lei Yu, Minghui Zhao, Li Zhu, Hong Zhang
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引用次数: 0
Mesangial Cell-Derived Extracellular Matrix Protein 1 Is Essential for Maintaining Mesangial Matrix Homeostasis and Glomerular Architecture. 系膜细胞衍生的细胞外基质蛋白1对维持系膜基质稳态和肾小球结构至关重要。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-12 DOI: 10.1681/ASN.0000000969
Pei Deng, Hui Zhou, Jieli Yu, Yinyin Li, Fang Yang, Danyan Zhang, Miaomiao Zhou, Jiao Luo, Lingling Gao, Enguang Bi, Nannan Guo, Jing Nie, Bing Sun, Fan Fan Hou, Yu Hu
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引用次数: 0
Genetic Determinants of Steroid Responsiveness in IgA Nephropathy. IgA肾病中类固醇反应性的遗传决定因素。
IF 9.4 1区 医学 Q1 UROLOGY & NEPHROLOGY Pub Date : 2025-12-11 DOI: 10.1681/ASN.0000000977
Lin-Lin Xu, Xu-Jie Zhou, Wenjian Bi, Peipei Zhang, Su-Fang Shi, Li-Jun Liu, Ji-Cheng Lv, Hong Zhang
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引用次数: 0
期刊
Journal of The American Society of Nephrology
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