@article{2076,
  keywords = {Cellular signalling networks, translational research},
  author = {Blue B. Lake and Rajasree Menon and Seth Winfree and Qiwen Hu and Ricardo Melo Ferreira and Kian Kalhor and Daria Barwinska and Edgar A. Otto and Michael Ferkowicz and Dinh Diep and Nongluk Plongthongkum and Amanda Knoten and Sarah Urata and Laura H. Mariani and Abhijit S. Naik and Sean Eddy and Bo Zhang and Yan Wu and Diane Salamon and James C. Williams and Xin Wang and Karol S. Balderrama and Paul J. Hoover and Evan Murray and Jamie L. Marshall and Teia Noel and Anitha Vijayan and Austin Hartman and Fei Chen and Sushrut S. Waikar and Sylvia E. Rosas and Francis P. Wilson and Paul M. Palevsky and Krzysztof Kiryluk and John R. Sedor and Robert D. Toto and Chirag R. Parikh and Eric H. Kim and Rahul Satija and Anna Greka and Evan Z. Macosko and Peter V. Kharchenko and Joseph P. Gaut and Jeffrey B. Hodgin and Michael T. Eadon and Pierre C. Dagher and Tarek M. El-Achkar and Kun Zhang and Matthias Kretzler and Sanjay Jain},
  title = {An atlas of healthy and injured cell states and niches in the human kidney},
  abstract = {Understanding kidney disease relies on defining the complexity of cell types and states, their associated molecular profiles and interactions within tissue neighbourhoods1. Here we applied multiple single-cell and single-nucleus assays (>400,000 nuclei or cells) and spatial imaging technologies to a broad spectrum of healthy reference kidneys (45 donors) and diseased kidneys (48 patients). This has provided a high-resolution cellular atlas of 51 main cell types, which include rare and previously undescribed cell populations. The multi-omic approach provides detailed transcriptomic profiles, regulatory factors and spatial localizations spanning the entire kidney. We also define 28 cellular states across nephron segments and interstitium that were altered in kidney injury, encompassing cycling, adaptive (successful or maladaptive repair), transitioning and degenerative states. Molecular signatures permitted the localization of these states within injury neighbourhoods using spatial transcriptomics, while large-scale 3D imaging analysis (around 1.2 million neighbourhoods) provided corresponding linkages to active immune responses. These analyses defined biological pathways that are relevant to injury time-course and niches, including signatures underlying epithelial repair that predicted maladaptive states associated with a decline in kidney function. This integrated multimodal spatial cell atlas of healthy and diseased human kidneys represents a comprehensive benchmark of cellular states, neighbourhoods, outcome-associated signatures and publicly available interactive visualizations.},
  year = {2023},
  journal = {Nature},
  volume = {619},
  pages = {585-594},
  month = {2023-07},
  issn = {1476-4687},
  url = {https://www.nature.com/articles/s41586-023-05769-3},
  doi = {10.1038/s41586-023-05769-3},
  language = {en},
}