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@ARTICLE{Micakovic:137573,
      author       = {T. Micakovic and S. Papagiannarou and E. Clark and Y. Kuzay
                      and K. Abramovic and J. Peters and C. Sticht and N. Volk and
                      T. Fleming and P. Nawroth and H.-P. Hammes and N. Alenina
                      and H.-J. Gröne$^*$ and S. C. Hoffmann},
      title        = {{T}he angiotensin {II} type 2 receptors protect renal
                      tubule mitochondria in early stages of diabetes mellitus.},
      journal      = {Kidney international},
      volume       = {94},
      number       = {5},
      issn         = {0085-2538},
      address      = {Basingstoke},
      publisher    = {Nature Publishing Group},
      reportid     = {DKFZ-2018-01453},
      pages        = {937-950},
      year         = {2018},
      abstract     = {Diabetic nephropathy correlates more closely to defective
                      mitochondria and increased oxidative stress in the kidney
                      than to hyperglycemia. A key driving factor of diabetic
                      nephropathy is angiotensin II acting via the
                      G-protein-coupled cell membrane type 1 receptor. The present
                      study aimed to investigate the role of the angiotensin II
                      type 2 receptor (AT2R) at the early stages of diabetic
                      nephropathy. Using receptor binding studies and
                      immunohistochemistry we found that the mitochondria in renal
                      tubules contain high-affinity AT2Rs. Increased renal
                      mitochondrial AT2R density by transgenic overexpression was
                      associated with reduced superoxide production of isolated
                      mitochondria from non-diabetic rats. Streptozotocin-induced
                      diabetes (28 days) caused a drop in the ATP/oxygen ratio and
                      an increase in the superoxide production of isolated renal
                      mitochondria from wild-type diabetic rats. This correlated
                      with changes in the renal expression profile and increased
                      tubular epithelial cell proliferation. AT2R overexpression
                      in tubular epithelial cells inhibited all diabetes-induced
                      renal changes including a drop in mitochondrial
                      bioenergetics efficiency, a rise in mitochondrial superoxide
                      production, metabolic reprogramming, and increased
                      proliferation. Thus, AT2Rs translocate to mitochondria and
                      can contribute to reno-protective effects at early stages of
                      diabetes. Hence, targeted AT2R overexpression in renal cells
                      may open new avenues to develop novel types of drugs
                      preventing diabetic nephropathy.},
      cin          = {G130},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331},
      pnm          = {322 - Genetics and Pathophysiology (POF3-322)},
      pid          = {G:(DE-HGF)POF3-322},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30190172},
      doi          = {10.1016/j.kint.2018.06.006},
      url          = {https://inrepo02.dkfz.de/record/137573},
}