Single-cell transcriptomics of the mouse kidney reveals potential cellular targets of kidney disease

  • Jihwan Park
    Renal Electrolyte and Hypertension Division, Department of Medicine and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Rojesh Shrestha
    Renal Electrolyte and Hypertension Division, Department of Medicine and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Chengxiang Qiu
    Renal Electrolyte and Hypertension Division, Department of Medicine and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Ayano Kondo
    Renal Electrolyte and Hypertension Division, Department of Medicine and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Shizheng Huang
    Renal Electrolyte and Hypertension Division, Department of Medicine and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Max Werth
    Renal Division, Department of Medicine, Columbia University, New York, NY 10032, USA.
  • Mingyao Li
    Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Jonathan Barasch
    Renal Division, Department of Medicine, Columbia University, New York, NY 10032, USA.
  • Katalin Suszták
    Renal Electrolyte and Hypertension Division, Department of Medicine and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA.

Description

<jats:title>Touring the kidney, cell by cell</jats:title> <jats:p> Our kidneys play a critical role in keeping us healthy, a fact of which we are reminded several times each day. This organ's cellular complexity has hindered progress in understanding the mechanisms underlying chronic kidney disease, which affects 10% of the world's population. Using single-cell transcriptional profiling, Park <jats:italic>et al.</jats:italic> produced a comprehensive cell atlas of the healthy mouse kidney (see the Perspective by Humphreys). An unexpected cell type in the collecting duct appears to be a transitional state between two known cell types. The transition from one cell type to the other is regulated by the Notch signaling pathway and is associated with metabolic acidosis. The authors also find that genetically distinct kidney diseases with common clinical features share common cellular origins. </jats:p> <jats:p> <jats:italic>Science</jats:italic> , this issue p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6390" page="758" related-article-type="in-this-issue" vol="360" xlink:href="10.1126/science.aar2131">758</jats:related-article> ; see also p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6390" page="709" related-article-type="in-this-issue" vol="360" xlink:href="10.1126/science.aat7271">709</jats:related-article> </jats:p>

Journal

  • Science

    Science 360 (6390), 758-763, 2018-05-18

    American Association for the Advancement of Science (AAAS)

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