Seminars in nephrology最新文献

Toward Combinatorial Strategies to Improve Proximal Tubule Recovery Following Acute Kidney Injury. 改善急性肾损伤后近端小管恢复的组合策略探讨。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-10-10 DOI: 10.1016/j.semnephrol.2025.151675

David A Bastos, Lisa O Oti, Carla L Ellis, Shayna T J Bradford

{"title":"Toward Combinatorial Strategies to Improve Proximal Tubule Recovery Following Acute Kidney Injury.","authors":"David A Bastos, Lisa O Oti, Carla L Ellis, Shayna T J Bradford","doi":"10.1016/j.semnephrol.2025.151675","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2025.151675","url":null,"abstract":"Maintaining kidney health throughout the human lifespan remains a significant global challenge. Worldwide, an estimated 850 million people have some level of kidney disease, with many unaware because of asymptomatic progression. Whether initiated by acute or chronic insults, renal injury and disease can have life-threatening consequences requiring interventions spanning the gamut of supportive care to kidney replacement therapies. Design of precision therapeutics is likely to benefit from understanding the heterogenous cell types and states that arise in the context of kidney injury and disease. Here we review an array of cellular states that have been detected following acute ischemic kidney injury, hypothesized to promote transition to chronic kidney disease. We focused on studies describing the cellular states of the proximal tubule (PT), a segment of the nephron most vulnerable to ischemic injury. PT cells have been shown in preclinical animal studies to have a heterogeneous response to ischemic injury, including repaired and failed-repair cellular states, inter alia. We end by discussing targeting these cellular states and/or pathological processes. Semin Nephrol 36:x-xx © 20XX Elsevier Inc. All rights reserved.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151675"},"PeriodicalIF":3.5,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145275601","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuroimmune Regulation for Acute Kidney Injury Therapy: Insights Along the Path From Bench to Bedside. 急性肾损伤治疗的神经免疫调节：从实验到临床的见解。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-10-08 DOI: 10.1016/j.semnephrol.2025.151674

William T Nash, Mark D Okusa

引用次数: 0

Using Predictive Models and AI for AKI Research. 利用预测模型和人工智能进行AKI研究。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-10-08 DOI: 10.1016/j.semnephrol.2025.151673

Madhumitha Rajagopal, Lili Chan, Girish N Nadkarni

引用次数: 0

Lessons Learned From Large Animal Models of Trauma-Induced AKI. 创伤性AKI大型动物模型的经验教训。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-10-01 DOI: 10.1016/j.semnephrol.2025.151670

David M Burmeister, Julia N Nguyen, Ian J Stewart

引用次数: 0

Innovative Technologies for Kidney Research: Three-Dimensional Imaging and Quantification. 肾脏研究的创新技术：三维成像和量化。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-10-01 DOI: 10.1016/j.semnephrol.2025.151671

Sarah R McLarnon, Pierre-Emmanuel Y N'Guetta, Lori L O'Brien

引用次数: 0

Therapeutic Approaches Involving Mitochondria in the Treatment of Acute Kidney Injury. 涉及线粒体的急性肾损伤治疗方法。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-09-29 DOI: 10.1016/j.semnephrol.2025.151676

Prisha S Patel, Navjot S Pabla, Amandeep Bajwa

{"title":"Therapeutic Approaches Involving Mitochondria in the Treatment of Acute Kidney Injury.","authors":"Prisha S Patel, Navjot S Pabla, Amandeep Bajwa","doi":"10.1016/j.semnephrol.2025.151676","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2025.151676","url":null,"abstract":"Acute kidney injury (AKI) continues to pose a significant clinical burden, characterized by high morbidity and mortality rates. Emerging evidence has established mitochondrial dysfunction as a central driver in the pathogenesis of AKI, encompassing deficits in bioenergetics, excessive production of reactive oxygen species, and disruption of mitochondrial dynamics. Therapeutic interventions targeting mitochondrial pathways-most notably peptide-based agents such as SS-31-have demonstrated promising results in preclinical models. Recent discoveries have identified phospholipid scramblase 3 (PLSCR3) as an essential mediator of SS-31's mitochondrial protective effects, positioning it as a novel therapeutic target. This review synthesizes current mitochondrial-directed approaches for AKI, with a particular emphasis on the mechanistic role of PLSCR3 in maintaining mitochondrial homeostasis and injury responses. Despite encouraging data, mitochondrial therapies face several translational hurdles, including limited bioavailability, challenges in establishing effective dosing regimens, incomplete mechanistic understanding, and variability in efficacy across different experimental models. Moreover, concerns regarding cost, accessibility, and long-term safety remain unresolved, contributing to inconsistent outcomes in clinical trials. Herein we evaluate the emerging role of PLSCR3 as a potentially druggable mitochondrial target, supported by recent genetic, biochemical, and in vivo evidence, and discuss translational strategies that may bridge the gap between experimental promise and clinical application. Semin Nephrol 36:x-xx © 20XX Elsevier Inc. All rights reserved.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151676"},"PeriodicalIF":3.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nontraditional Models for Acute Kidney Injury Research: Organoids, Zebrafish, and More. 急性肾损伤研究的非传统模型：类器官、斑马鱼等。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-09-15 DOI: 10.1016/j.semnephrol.2025.151668

Eeshrita Jog, Tongyu Wu, Joseph C Maggiore, Neil A Hukriede

{"title":"Nontraditional Models for Acute Kidney Injury Research: Organoids, Zebrafish, and More.","authors":"Eeshrita Jog, Tongyu Wu, Joseph C Maggiore, Neil A Hukriede","doi":"10.1016/j.semnephrol.2025.151668","DOIUrl":"https://doi.org/10.1016/j.semnephrol.2025.151668","url":null,"abstract":"Acute kidney injury (AKI) is a condition that is associated with increased mortality in the clinic and currently has no Food and Drug Administration-approved drug intervention that prevents progression to chronic kidney disease. To address the lack of therapy, it is imperative to use multiple model systems that can recapitulate the complex pathophysiology of AKI. Rodent AKI models are the gold standard and are widely used, but their genetic, metabolic, and circadian cycle divergence from humans can create hurdles in translational research. Similarly, well-established two-dimensional cell lines lack the complexity necessary to model heterogeneous injury occurring in multiple distinct renal cell types during AKI events. Advances in three-dimensional kidney organoids and microfluidic model systems are increasingly bridging the gap by improving structural and functional similarities to human renal tissue. Zebrafish and Drosophila models also provide functionally relevant systems that allow for high-content screening capabilities in whole organisms. In this review, we summarize three-dimensional in vitro and nonmammalian model systems and discuss how these systems have provided researchers with valuable platforms for furthering AKI drug discovery efforts.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151668"},"PeriodicalIF":3.5,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145075988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Myeloid Cells in Acute Kidney Injury. 髓系细胞在急性肾损伤中的作用。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-09-13 DOI: 10.1016/j.semnephrol.2025.151666

Yohan Park, Kurt A Zimmerman, Sarah J Miller

引用次数: 0

When the Heart Hurts the Kidneys: From Flow to Translational Future. 当心脏伤害肾脏：从流动到翻译的未来。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-09-10 DOI: 10.1016/j.semnephrol.2025.151667

Kevin G Burfeind, Daiki Aomura, Jessica F Hebert, Michael P Hutchens

引用次数: 0

The Clinical View of Sepsis-Associated AKI: How Basic Science Can Help Solve This Problem. 败血症相关AKI的临床观点：基础科学如何帮助解决这一问题。

IF 3.5 3区医学

Seminars in nephrology Pub Date : 2025-09-10 DOI: 10.1016/j.semnephrol.2025.151665

James D Odum, Denise C Hasson, Natalja L Stanski, Hernando Gómez, Danielle E Soranno

{"title":"The Clinical View of Sepsis-Associated AKI: How Basic Science Can Help Solve This Problem.","authors":"James D Odum, Denise C Hasson, Natalja L Stanski, Hernando Gómez, Danielle E Soranno","doi":"10.1016/j.semnephrol.2025.151665","DOIUrl":"10.1016/j.semnephrol.2025.151665","url":null,"abstract":"The global health impact of sepsis is difficult to understate. As a complication of sepsis, the development of sepsis-associated acute kidney injury (SA-AKI) significantly increases the risk of mortality. Although several epidemiological risk factors for SA-AKI are known, the heterogeneity of this syndrome-across patients, pathogens, and treatment responses-has hindered therapeutic innovation and contributed to persistently poor outcomes. Precision medicine offers a promising framework to address this complexity, yet a substantial translational gap remains between mechanistic insights from preclinical models and the therapeutic strategies used in clinical practice. To bridge this gap, researchers should consider aligning preclinical models with human sepsis and embrace SA-AKI heterogeneity to identify treatable, mechanistically informed subtypes (endotypes). These efforts could enable the development of personalized therapies aimed at reducing the burden of SA-AKI. Semin Nephrol 36:x-xx © 20XX Elsevier Inc. All rights reserved.","PeriodicalId":21756,"journal":{"name":"Seminars in nephrology","volume":" ","pages":"151665"},"PeriodicalIF":3.5,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145041365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0