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@ARTICLE{Chen:166579,
      author       = {J. Chen and T. Fleming and S. Katz and M. Dewenter and K.
                      Hofmann and A. Saadatmand and M. Kronlage and M. P. Werner
                      and B. Pokrandt and F. Schreiter and J. Lin and D. Katz and
                      J. Morgenstern and A. Elwakiel and P. Sinn and H.-J.
                      Gröne$^*$ and H.-P. Hammes and P. P. Nawroth and B.
                      Isermann and C. Sticht and B. Brügger and H. A. Katus and
                      M. Hagenmueller and J. Backs},
      title        = {{C}a{M} {K}inase {II}-δ is {R}equired for {D}iabetic
                      {H}yperglycemia and {R}etinopathy but not {N}ephropathy.},
      journal      = {Diabetes},
      volume       = {70},
      number       = {2},
      issn         = {1939-327X},
      address      = {Alexandria, Va},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2020-03022},
      pages        = {616-626},
      year         = {2021},
      note         = {2021 Feb;70(2):616-626},
      abstract     = {Type 2 diabetes has become a pandemic and leads to late
                      diabetic complications of organs including kidney and eye.
                      Lowering hyperglycemia is the typical therapeutic goal in
                      clinical medicine. However, hyperglycemia may only be a
                      symptom of diabetes but not the sole cause of late diabetic
                      complications, Instead, other diabetes-related alterations
                      could be causative. Here, we studied the role of CaM Kinase
                      II δ (CaMKIIδ) that is known to be activated through
                      diabetic metabolism. CaMKIIδ is expressed ubiquitously and
                      might therefore affect several different organ systems. We
                      crossed diabetic leptin receptor mutant mice to mice lacking
                      CaMKIIδ globally. Remarkably, CaMKIIδ-deficient diabetic
                      mice did not develop hyperglycemia. As potential underlying
                      mechanisms, we provide evidence for improved insulin sensing
                      with increased glucose transport into skeletal muscle but
                      also reduced hepatic glucose production. Despite
                      normoglycemia, CaMKIIδ-deficient diabetic mice developed
                      the full picture of diabetic nephropathy but diabetic
                      retinopathy was prevented. We also unmasked a
                      retina-specific gene expression signature that might
                      contribute to CaMKII-dependent retinal diabetic
                      complications. These data challenge the clinical concept of
                      normalizing hyperglycemia in diabetes as a causative
                      treatment strategy for late diabetic complications and call
                      for a more detailed analysis of intracellular metabolic
                      signals in different diabetic organs.},
      cin          = {G130},
      ddc          = {610},
      cid          = {I:(DE-He78)G130-20160331},
      pnm          = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
      pid          = {G:(DE-HGF)POF4-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33239449},
      doi          = {10.2337/db19-0659},
      url          = {https://inrepo02.dkfz.de/record/166579},
}