What We Have Learned so far From Single Cell Sequencing in Acute Kidney Injury

Buse, Marc; Moeller, Marcus J.; Stamellou, Eleni

doi:10.3389/fphys.2022.933677

Cited by 3 publications

(3 citation statements)

References 36 publications

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“…and Gerhardt et al. described a cell population, termed “failed-repair PTs” or “maladaptive PTs.” 19 , 36 , 37 These cells appeared late in the course of injury and were characterized by the up-regulation of a new distinct set of genes such as Vcam -1, Ccl2, Pdgfd, and down-regulation of terminal differentiation genes. They acquired a proinflammatory and profibrotic phenotype, and it has been suggested that they may be involved in the progression from AKI to CKD.…”

Section: Discussionmentioning

confidence: 99%

Lineage tracing reveals transient phenotypic adaptation of tubular cells during acute kidney injury

Buse,

Cheng,

Jankowski

et al. 2024

iScience

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Section: Discussionmentioning

confidence: 99%

Lineage tracing reveals transient phenotypic adaptation of tubular cells during acute kidney injury

Buse,

Cheng,

Jankowski

et al. 2024

iScience

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“…To date, mechanistic factors enabling productive, adaptive repair versus persistent, maladaptive injury states remain poorly understood and are the focus of active research. In particular, a lot of progress has been made through the application of single-cell technologies and spatial transcriptomics in mouse models of I/R injury [63,64]. For example, single-nucleus RNA sequencing identified distinct, late-stage injury, proximal tubule cell states (Vcam1 + /Ccl2 + with upregulation of NFκB, tumor necrosis factor, and AP-1 signaling pathways) associated with the AKI-CKD transition and SASP [65][66][67].…”

Section: Cellular Adaptive and Maladaptive Repairmentioning

confidence: 99%

“…We believe that the current implementation of multiomics research (genomics, transcriptomics, metabolomics, and proteomics) holds great potential to improve our insights on these matters. From single-cell and spatial transcriptomics we have already acquired a better understanding of adaptive and maladaptive repair after acute kidney injury [63].…”

Section: Challenges and Future Considerationsmentioning

confidence: 99%

How to Best Protect Kidneys for Transplantation—Mechanistic Target

Akalay

Hosgood

2023

JCM

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The increasing number of patients on the kidney transplant waiting list underlines the need to expand the donor pool and improve kidney graft utilization. By protecting kidney grafts adequately from the initial ischemic and subsequent reperfusion injury occurring during transplantation, both the number and quality of kidney grafts could be improved. The last few years have seen the emergence of many new technologies to abrogate ischemia–reperfusion (I/R) injury, including dynamic organ preservation through machine perfusion and organ reconditioning therapies. Although machine perfusion is gradually making the transition to clinical practice, reconditioning therapies have not yet progressed from the experimental setting, pointing towards a translational gap. In this review, we discuss the current knowledge on the biological processes implicated in I/R injury and explore the strategies and interventions that are being proposed to either prevent I/R injury, treat its deleterious consequences, or support the reparative response of the kidney. Prospects to improve the clinical translation of these therapies are discussed with a particular focus on the need to address multiple aspects of I/R injury to achieve robust and long-lasting protective effects on the kidney graft.

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Gender and Renal Insufficiency: Opportunities for Their Therapeutic Management?

Ciarambino

Giordano

2022

Cells

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Acute kidney injury (AKI) is a major clinical problem associated with increased morbidity and mortality. Despite intensive research, the clinical outcome remains poor, and apart from supportive therapy, no other specific therapy exists. Furthermore, acute kidney injury increases the risk of developing chronic kidney disease (CKD) and end-stage renal disease. Acute tubular injury accounts for the most common intrinsic cause of AKI. The main site of injury is the proximal tubule due to its high workload and energy demand. Upon injury, an intratubular subpopulation of proximal epithelial cells proliferates and restores the tubular integrity. Nevertheless, despite its strong regenerative capacity, the kidney does not always achieve its former integrity and function and incomplete recovery leads to persistent and progressive CKD. Clinical and experimental data demonstrate sexual differences in renal anatomy, physiology, and susceptibility to renal diseases including but not limited to ischemia-reperfusion injury. Some data suggest the protective role of female sex hormones, whereas others highlight the detrimental effect of male hormones in renal ischemia-reperfusion injury. Although the important role of sex hormones is evident, the exact underlying mechanisms remain to be elucidated. This review focuses on collecting the current knowledge about sexual dimorphism in renal injury and opportunities for therapeutic manipulation, with a focus on resident renal progenitor stem cells as potential novel therapeutic strategies.

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What We Have Learned so far From Single Cell Sequencing in Acute Kidney Injury

Cited by 3 publications

References 36 publications

Lineage tracing reveals transient phenotypic adaptation of tubular cells during acute kidney injury

Lineage tracing reveals transient phenotypic adaptation of tubular cells during acute kidney injury

How to Best Protect Kidneys for Transplantation—Mechanistic Target

Gender and Renal Insufficiency: Opportunities for Their Therapeutic Management?

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