Mapping the human kidney using single-cell genomics

Schreibing, Felix; Kramann, Rafael

doi:10.1038/s41581-022-00553-4

Cited by 54 publications

(35 citation statements)

References 105 publications

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“…To distinguish myofibroblasts, vimentin, collagen-1α1 (Col1a1), CD73, plateletderived growth factor receptor beta (PDGFRβ), and fibroblastspecific protein-1 (FSP1)/S100A4 could be used. 10,12 The number of myofibroblast is rare in normal condition, but increases sharply in fibrotic kidneys. However, the origin of myofibroblast remains controversial.…”

Section: Myofibroblastmentioning

confidence: 99%

“…11 In particular, the rapidly developing technologies of spatial and single-cell transcriptomics could facilitate dissecting genetic programming, signal pathway, and the mechanism of cell crosstalk that underlie kidney function in physiological conditions, as well as the dysfunctions in fibrotic condition. 12 Epigenetics controls gene expression without altering DNA sequence and affect the gene and environment crosstalk. 13 Epigenetic regulation exerted fundamental and crucial functions in cell biology of kidneys through the action of DNA methylation, chromatin modifications via epigenetic factors and interaction with transcription factors, and non-coding RNAs.…”

Section: Introductionmentioning

confidence: 99%

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Kidney fibrosis: from mechanisms to therapeutic medicines

Huang

2023

Sig Transduct Target Ther

176

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Chronic kidney disease (CKD) is estimated to affect 10–14% of global population. Kidney fibrosis, characterized by excessive extracellular matrix deposition leading to scarring, is a hallmark manifestation in different progressive CKD; However, at present no antifibrotic therapies against CKD exist. Kidney fibrosis is identified by tubule atrophy, interstitial chronic inflammation and fibrogenesis, glomerulosclerosis, and vascular rarefaction. Fibrotic niche, where organ fibrosis initiates, is a complex interplay between injured parenchyma (like tubular cells) and multiple non-parenchymal cell lineages (immune and mesenchymal cells) located spatially within scarring areas. Although the mechanisms of kidney fibrosis are complicated due to the kinds of cells involved, with the help of single-cell technology, many key questions have been explored, such as what kind of renal tubules are profibrotic, where myofibroblasts originate, which immune cells are involved, and how cells communicate with each other. In addition, genetics and epigenetics are deeper mechanisms that regulate kidney fibrosis. And the reversible nature of epigenetic changes including DNA methylation, RNA interference, and chromatin remodeling, gives an opportunity to stop or reverse kidney fibrosis by therapeutic strategies. More marketed (e.g., RAS blockage, SGLT2 inhibitors) have been developed to delay CKD progression in recent years. Furthermore, a better understanding of renal fibrosis is also favored to discover biomarkers of fibrotic injury. In the review, we update recent advances in the mechanism of renal fibrosis and summarize novel biomarkers and antifibrotic treatment for CKD.

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Section: Myofibroblastmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Kidney fibrosis: from mechanisms to therapeutic medicines

Huang

2023

Sig Transduct Target Ther

176

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“…[1][2][3] The tremendous benefits for research areas from cancer genomics to developmental biology became obvious when these approaches developed from ultra-lowinput protocols for few single cells to highly scalable assays that enabled the investigation of the (patho-)physiology of complex organ systems. [4][5][6] A recent review article on single cell technologies applied to the human kidney 7 highlights the enormous impact on research in the field of physiology. Here, single cell technology-based studies are reviewed that dissect the genetic programs, pathways, and mechanisms of cellular crosstalk underlying physiological kidney development and function, as well as the changes that occur in different pathological conditions.…”

Section: Cell Technologiesmentioning

confidence: 99%

Single cell‐ and spatial ‘Omics revolutionize physiology

Conrad

Altmüller

2022

Acta Physiologica

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Single cell multi‐ ‘Omics and Spatial Transcriptomics are prominent technological highlights of recent years, and both fields still witness a ceaseless firework of novel approaches for high resolution profiling of additional omics layers. As all life processes in organs and organisms are based on the functions of their fundamental building blocks, the individual cells and their interactions, these methods are of utmost worth for the study of physiology in health and disease. Recent discoveries on embryonic development, tumor immunology, the detailed cellular composition and function of complex tissues like for example the kidney or the brain, different roles of the same cell type in different organs, the oncogenic program of individual tumor entities, or the architecture of immunopathology in infected tissue are based on single cell and spatial transcriptomics experiments. In this review, we will give a broad overview of technological concepts for single cell and spatial analysis, showing both advantages and limitations, and illustrate their impact with some particularly impressive case studies.

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“…Kidney disease is a complex, highly prevalent and fatal disease with a heavy socio‐economic burden. Although many studies have been conducted to advance our understanding of kidney diseases, the research to date is insufficient to explain the specific mechanisms and establish the desired therapeutic strategies (Schreibing & Kramann, 2022). Therefore, we need to conduct more in‐depth research to explore and address the above deficiencies.…”

Section: Introductionmentioning

confidence: 99%

RNA N⁶‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease

et al. 2022

British J Pharmacology

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Epigenetic modifications have received increasing attention and have been shown to be extensively involved in kidney development and disease progression. Among them, the most common RNA modification, N6‐methyladenosine (m6A), has been shown to dynamically and reversibly exert its functions in multiple ways, including splicing, export, decay and translation initiation efficiency to regulate mRNA fate. Moreover, m6A has also been reported to exert biological effects by destabilizing base pairing to modulate various functions of RNAs. Most importantly, an increasing number of kidney diseases, such as renal cell carcinoma, acute kidney injury and chronic kidney disease, have been found to be associated with aberrant m6A patterns. In this review, we comprehensively review the critical roles of m6A in kidney diseases and discuss the possibilities and relevance of m6A‐targeted epigenetic therapy, with an integrated comprehensive description of the detailed alterations in specific loci that contribute to cellular processes that are associated with kidney diseases.

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Mapping the human kidney using single-cell genomics

Cited by 54 publications

References 105 publications

Kidney fibrosis: from mechanisms to therapeutic medicines

Kidney fibrosis: from mechanisms to therapeutic medicines

Single cell‐ and spatial ‘Omics revolutionize physiology

RNA N⁶‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease

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Mapping the human kidney using single-cell genomics

Cited by 54 publications

References 105 publications

Kidney fibrosis: from mechanisms to therapeutic medicines

Kidney fibrosis: from mechanisms to therapeutic medicines

Single cell‐ and spatial ‘Omics revolutionize physiology

RNA N6‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease

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RNA N⁶‐methyladenosine modifications and potential targeted therapeutic strategies in kidney disease