@article{JohnGruneOttetal.2018,
  author    = {John, Cathleen and Grune, Jana and Ott, Christiane and Nowotny, Kerstin and Deubel, Stefanie and K{\"u}hne, Arne and Schubert, Carola and Kintscher, Ulrich and Regitz-Zagrosek, Vera and Grune, Tilman},
  title     = {Sex Differences in Cardiac Mitochondria in the New Zealand Obese Mouse},
  series = {Frontiers in Endocrinology},
  volume    = {9},
  journal   = {Frontiers in Endocrinology},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1664-2392},
  doi       = {10.3389/fendo.2018.00732},
  pages     = {9},
  year      = {2018},
  abstract  = {Background: Obesity is a risk factor for diseases including type 2 diabetes mellitus (T2DM) and cardiovascular disorders. Diabetes itself contributes to cardiac damage. Thus, studying cardiovascular events and establishing therapeutic intervention in the period of type T2DM onset and manifestation are of highest importance. Mitochondrial dysfunction is one of the pathophysiological mechanisms leading to impaired cardiac function. Methods: An adequate animal model for studying pathophysiology of T2DM is the New Zealand Obese (NZO) mouse. These mice were maintained on a high-fat diet (HFD) without carbohydrates for 13 weeks followed by 4 week HFD with carbohydrates. NZO mice developed severe obesity and only male mice developed manifest T2DM. We determined cardiac phenotypes and mitochondrial function as well as cardiomyocyte signaling in this model. Results: The development of an obese phenotype and T2DM in male mice was accompanied by an impaired systolic function as judged by echocardiography and MyH6/7 expression. Moreover, the mitochondrial function only in male NZO hearts was significantly reduced and ERK1/2 and AMPK protein levels were altered. Conclusions: This is the first report demonstrating that the cardiac phenotype in male diabetic NZO mice is associated with impaired cardiac energy function and signaling events.},
  language  = {en}
}
@article{NordmeyerKrausZiehmetal.2023,
  author    = {Nordmeyer, Sarah and Kraus, Milena and Ziehm, Matthias and Kirchner, Marieluise and Schafstedde, Marie and Kelm, Marcus and Niquet, Sylvia and Stephen, Mariet Mathew and Baczko, Istvan and Knosalla, Christoph and Schapranow, Matthieu-Patrick and Dittmar, Gunnar and Gotthardt, Michael and Falcke, Martin and Regitz-Zagrosek, Vera and Kuehne, Titus and Mertins, Philipp},
  title     = {Disease- and sex-specific differences in patients with heart valve disease},
  series = {Life Science Alliance},
  volume    = {6},
  journal   = {Life Science Alliance},
  number    = {3},
  publisher = {EMBO Press},
  address   = {Heidelberg},
  issn      = {2575-1077},
  doi       = {10.26508/lsa.202201411},
  pages     = {18},
  year      = {2023},
  abstract  = {Pressure overload in patients with aortic valve stenosis and volume overload in mitral valve regurgitation trigger specific forms of cardiac remodeling; however, little is known about similarities and differences in myocardial proteome regulation. We performed proteome profiling of 75 human left ventricular myocardial biopsies (aortic stenosis = 41, mitral regurgitation = 17, and controls = 17) using high-resolution tandem mass spectrometry next to clinical and hemodynamic parameter acquisition. In patients of both disease groups, proteins related to ECM and cytoskeleton were more abundant, whereas those related to energy metabolism and proteostasis were less abundant compared with controls. In addition, disease group-specific and sex-specific differences have been observed. Male patients with aortic stenosis showed more proteins related to fibrosis and less to energy metabolism, whereas female patients showed strong reduction in proteostasis-related proteins. Clinical imaging was in line with proteomic findings, showing elevation of fibrosis in both patient groups and sex differences. Disease-and sex-specific proteomic profiles provide insight into cardiac remodeling in patients with heart valve disease and might help improve the understanding of molecular mechanisms and the development of individualized treatment strategies.},
  language  = {en}
}