Jonathan M. Barasch

About

Jonathan M. Barasch, MD, PhD, is the Samuel W. Lambert Professor of Medicine and Pathology and Cell Biology at Columbia University Irving Medical Center. His research focuses on kidney development, specifically the mechanisms that produce the epithelial phenotype during mesenchymal to epithelial conversion in nephrogenesis. He investigates the interaction of ureteric bud and metanephric mesenchyme, identifying factors secreted from the ureteric bud that stimulate mesenchymal cell conversion into epithelia, tubules, and nephrons. His work includes the identification of inductive molecules such as Leukemia Inhibitory Factor (LIF) and siderocalin (lipocalin-2), exploring their roles in kidney growth, nephrogenesis, and response to nephrotoxins or ischemia. Dr. Barasch's research aims to uncover novel cytokines, receptors, and gene regulators involved in kidney epithelial development, contributing to the understanding of renal morphogenesis and potential therapeutic targets for kidney injury.

Research topics

• Biology
• Medicine
• Internal medicine
• Cell biology
• Pathology
• Genetics
• Biochemistry
• Evolutionary biology
• Computational biology
• Biophysics

Selected publications

• An atlas of healthy and injured cell states and niches in the human kidney

  Nature · 2023 · 631 citations

  . 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.…

  PublisherOA PDFDOI

• Kidney Biopsy Findings in Patients with COVID-19

  Journal of the American Society of Nephrology · 2020 · 421 citations

  BACKGROUND: Coronavirus disease 2019 (COVID-19) is thought to cause kidney injury by a variety of mechanisms. To date, pathologic analyses have been limited to patient reports and autopsy series. METHODS: hybridization, and electron microscopy to examine this tissue for presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). RESULTS: high-risk gene variants. We found no definitive evidence of SARS-CoV-2 in kidney cells. Biopsy diagnosis informed treatment and prognosis in all p…

  DOI

• Postmortem Kidney Pathology Findings in Patients with COVID-19

  Journal of the American Society of Nephrology · 2020 · 317 citations

  BACKGROUND: AKI is common among hospitalized patients with coronavirus disease 2019 (COVID-19) and is an independent risk factor for mortality. Although there are numerous potential mechanisms underlying COVID-19-associated AKI, our current knowledge of kidney pathologic findings in COVID-19 is limited. METHODS: hybridization studies for SARS-CoV-2 on a subset of samples. RESULTS: hybridization for SARS-CoV-2 showed no definitive positivity. CONCLUSIONS: Among a cohort of 42 patients dying with…

  DOI

• Structures of LRP2 reveal a molecular machine for endocytosis

  Cell · 2023 · 69 citations

  PublisherOA PDFDOI

• The mitochondrial metal transporters mitoferrin1 and mitoferrin2 are required for liver regeneration and cell proliferation in mice

  Journal of Biological Chemistry · 2020 · 60 citations

  were unable to proliferate, and overexpression of Mfrn1-GFP or Mfrn2-GFP prevented this proliferation defect. Loss of both mitoferrins in hepatocytes dramatically reduced regeneration in the adult mouse liver, further supporting the notion that both mitoferrins transport iron and that their absence limits proliferative capacity of mammalian cells. We conclude that Mfrn1 and Mfrn2 contribute to mitochondrial iron homeostasis and are required for high-affinity iron import during active proliferati…

  PublisherOA PDFDOI

Recent grants

• NIH Grant P01DK055388

  NIH · $21.1M · 2008

• NIH Grant R01DK092684

  NIH · $1.7M · 2018

• A Novel Metabolic Pathway Regulates Urinary Tract Infections in the Bladder

  NIH · $3.4M · 2014–2019

Frequent coauthors

• Kai M. Schmidt‐Ott

  Medizinische Hochschule Hannover

  55 shared

• Prasad Devarajan

  Cincinnati Children's Hospital Medical Center

  55 shared

• Jun Yang

  Dalian Medical University

  37 shared

• Kiyoshi Mori

  36 shared

• Thomas L. Nickolas

  Columbia University Irving Medical Center

  35 shared

• Sushrut S. Waikar

  Boston University

  34 shared

• Vivette D. D’Agati

  Columbia University Irving Medical Center

  34 shared

• Michael T. Eadon

  Indiana University School of Medicine

  29 shared

Education

• M.D.

  Columbia University

• Ph.D.

  Columbia University

Awards & honors

• Shelanski Research Innovation Award in Pathology

Similar researchers at Columbia University

• Ottavio Arancioh-95
• Rando L. Allikmetsh-79
• Bachir Alobeidh-37