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@ARTICLE{Garreta:180319,
      author       = {E. Garreta and P. Prado and M. L. Stanifer$^*$ and V.
                      Monteil and A. Marco and A. Ullate-Agote and D. Moya-Rull
                      and A. Vilas-Zornoza and C. Tarantino and J. P. Romero and
                      G. Jonsson and R. Oria and A. Leopoldi and A. Hagelkruys and
                      M. Gallo and F. González and P. Domingo-Pedrol and A.
                      Gavaldà and C. H. Del Pozo and O. Hasan Ali and P.
                      Ventura-Aguiar and J. M. Campistol and F. Prosper and A.
                      Mirazimi and S. Boulant$^*$ and J. M. Penninger and N.
                      Montserrat},
      title        = {{A} diabetic milieu increases {ACE}2 expression and
                      cellular susceptibility to {SARS}-{C}o{V}-2 infections in
                      human kidney organoids and patient cells.},
      journal      = {Cell metabolism},
      volume       = {34},
      number       = {6},
      issn         = {1550-4131},
      address      = {Cambridge, Mass.},
      publisher    = {Cell Press},
      reportid     = {DKFZ-2022-01246},
      pages        = {857 - 873.e9},
      year         = {2022},
      abstract     = {It is not well understood why diabetic individuals are more
                      prone to develop severe COVID-19. To this, we here
                      established a human kidney organoid model promoting early
                      hallmarks of diabetic kidney disease development. Upon
                      SARS-CoV-2 infection, diabetic-like kidney organoids
                      exhibited higher viral loads compared with their control
                      counterparts. Genetic deletion of the angiotensin-converting
                      enzyme 2 (ACE2) in kidney organoids under control or
                      diabetic-like conditions prevented viral detection.
                      Moreover, cells isolated from kidney biopsies from diabetic
                      patients exhibited altered mitochondrial respiration and
                      enhanced glycolysis, resulting in higher SARS-CoV-2
                      infections compared with non-diabetic cells. Conversely, the
                      exposure of patient cells to dichloroacetate (DCA), an
                      inhibitor of aerobic glycolysis, resulted in reduced
                      SARS-CoV-2 infections. Our results provide insights into the
                      identification of diabetic-induced metabolic programming in
                      the kidney as a critical event increasing SARS-CoV-2
                      infection susceptibility, opening the door to the
                      identification of new interventions in COVID-19 pathogenesis
                      targeting energy metabolism.},
      keywords     = {Angiotensin-Converting Enzyme 2 / COVID-19 / Diabetes
                      Mellitus / Diabetic Nephropathies / Humans / Kidney:
                      metabolism / Organoids / Peptidyl-Dipeptidase A: genetics /
                      Peptidyl-Dipeptidase A: metabolism / SARS-CoV-2 / ACE2
                      (Other) / COVID-19 (Other) / SARS-CoV-2 (Other) /
                      angiotensin-converting enzyme 2 (Other) / diabetes 2 (Other)
                      / human kidney organoids (Other) / Peptidyl-Dipeptidase A
                      (NLM Chemicals) / Angiotensin-Converting Enzyme 2 (NLM
                      Chemicals)},
      cin          = {F140},
      ddc          = {570},
      cid          = {I:(DE-He78)F140-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35561674},
      pmc          = {pmc:PMC9097013},
      doi          = {10.1016/j.cmet.2022.04.009},
      url          = {https://inrepo02.dkfz.de/record/180319},
}