Anaerobic Glycolysis Maintains the Glomerular Filtration Barrier Independent of Mitochondrial Metabolism and Dynamics

Paul T. Brinkkoetter(University of Cologne), Tillmann Bork(University of Freiburg), Sarah Salou(University of Freiburg), Wei Liang(University of Freiburg), Athanasia Mizi(University of Cologne), Cem Özel(University of Cologne), Sybille Koehler(University of Cologne), Henning Hagmann(University of Cologne), Christina Ising(University of Cologne), Alexander Kuczkowski(University of Cologne), Svenia Schnyder(University of Basel), Ahmed Abed(University of Freiburg), Bernhard Schermer(University of Cologne), Thomas Benzing(University of Cologne), Oliver Kretz(Universität Hamburg), Victor G. Puelles(Universität Hamburg), Simon Lagies(University of Freiburg), Manuel Schlimpert(University of Freiburg), Bernd Kammerer(University of Freiburg), Christoph Handschin(University of Basel), Christoph Schell(University of Freiburg), Tobias B. Huber(Universität Hamburg)
Cell Reports
April 1, 2019
Cited by 166Open Access
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Abstract

The cellular responses induced by mitochondrial dysfunction remain elusive. Intrigued by the lack of almost any glomerular phenotype in patients with profound renal ischemia, we comprehensively investigated the primary sources of energy of glomerular podocytes. Combining functional measurements of oxygen consumption rates, glomerular metabolite analysis, and determination of mitochondrial density of podocytes in vivo, we demonstrate that anaerobic glycolysis and fermentation of glucose to lactate represent the key energy source of podocytes. Under physiological conditions, we could detect neither a developmental nor late-onset pathological phenotype in podocytes with impaired mitochondrial biogenesis machinery, defective mitochondrial fusion-fission apparatus, or reduced mtDNA stability and transcription caused by podocyte-specific deletion of Pgc-1α, Drp1, or Tfam, respectively. Anaerobic glycolysis represents the predominant metabolic pathway of podocytes. These findings offer a strategy to therapeutically interfere with the enhanced podocyte metabolism in various progressive kidney diseases, such as diabetic nephropathy or focal segmental glomerulosclerosis (FSGS).


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