@article{HuberLeziusReibisetal.2015,
  author    = {Huber, Matthias and Lezius, Susanne and Reibis, Rona Katharina and Treszl, Andras and Kujawinska, Dorota and Jakob, Stefanie and Wegscheider, Karl and V{\"o}ller, Heinz and Kreutz, Reinhold},
  title     = {A Single Nucleotide Polymorphism near the CYP17A1 Gene Is Associated with Left Ventricular Mass in Hypertensive Patients under Pharmacotherapy},
  series = {International journal of molecular sciences},
  volume    = {16},
  journal   = {International journal of molecular sciences},
  number    = {8},
  publisher = {MDPI},
  address   = {Basel},
  issn      = {1422-0067},
  doi       = {10.3390/ijms160817456},
  pages     = {17456 -- 17468},
  year      = {2015},
  abstract  = {Cytochrome P450 17A1 (CYP17A1) catalyses the formation and metabolism of steroid hormones. They are involved in blood pressure (BP) regulation and in the pathogenesis of left ventricular hypertrophy. Therefore, altered function of CYP17A1 due to genetic variants may influence BP and left ventricular mass. Notably, genome wide association studies supported the role of this enzyme in BP control. Against this background, we investigated associations between single nucleotide polymorphisms (SNPs) in or nearby the CYP17A1 gene with BP and left ventricular mass in patients with arterial hypertension and associated cardiovascular organ damage treated according to guidelines. Patients (n = 1007, mean age 58.0 +/- 9.8 years, 83\% men) with arterial hypertension and cardiac left ventricular ejection fraction (LVEF) 40\% were enrolled in the study. Cardiac parameters of left ventricular mass, geometry and function were determined by echocardiography. The cohort comprised patients with coronary heart disease (n = 823; 81.7\%) and myocardial infarction (n = 545; 54.1\%) with a mean LVEF of 59.9\% +/- 9.3\%. The mean left ventricular mass index (LVMI) was 52.1 +/- 21.2 g/m(2.7) and 485 (48.2\%) patients had left ventricular hypertrophy. There was no significant association of any investigated SNP (rs619824, rs743572, rs1004467, rs11191548, rs17115100) with mean 24 h systolic or diastolic BP. However, carriers of the rs11191548 C allele demonstrated a 7\% increase in LVMI (95\% CI: 1\%-12\%, p = 0.017) compared to non-carriers. The CYP17A1 polymorphism rs11191548 demonstrated a significant association with LVMI in patients with arterial hypertension and preserved LVEF. Thus, CYP17A1 may contribute to cardiac hypertrophy in this clinical condition.},
  language  = {en}
}
@article{KoenigAblerAgartzetal.2020,
  author    = {Koenig, Julian and Abler, Birgit and Agartz, Ingrid and akerstedt, Torbjorn and Andreassen, Ole A. and Anthony, Mia and Baer, Karl-Juergen and Bertsch, Katja and Brown, Rebecca C. and Brunner, Romuald and Carnevali, Luca and Critchley, Hugo D. and Cullen, Kathryn R. and de Geus, Eco J. C. and de la Cruz, Feliberto and Dziobek, Isabel and Ferger, Marc D. and Fischer, Hakan and Flor, Herta and Gaebler, Michael and Gianaros, Peter J. and Giummarra, Melita J. and Greening, Steven G. and Guendelman, Simon and Heathers, James A. J. and Herpertz, Sabine C. and Hu, Mandy X. and Jentschke, Sebastian and Kaess, Michael and Kaufmann, Tobias and Klimes-Dougan, Bonnie and Koelsch, Stefan and Krauch, Marlene and Kumral, Deniz and Lamers, Femke and Lee, Tae-Ho and Lekander, Mats and Lin, Feng and Lotze, Martin and Makovac, Elena and Mancini, Matteo and Mancke, Falk and Mansson, Kristoffer N. T. and Manuck, Stephen B. and Mather, Mara and Meeten, Frances and Min, Jungwon and Mueller, Bryon and Muench, Vera and Nees, Frauke and Nga, Lin and Nilsonne, Gustav and Ordonez Acuna, Daniela and Osnes, Berge and Ottaviani, Cristina and Penninx, Brenda W. J. H. and Ponzio, Allison and Poudel, Govinda R. and Reinelt, Janis and Ren, Ping and Sakaki, Michiko and Schumann, Andy and Sorensen, Lin and Specht, Karsten and Straub, Joana and Tamm, Sandra and Thai, Michelle and Thayer, Julian F. and Ubani, Benjamin and van Der Mee, Denise J. and van Velzen, Laura S. and Ventura-Bort, Carlos and Villringer, Arno and Watson, David R. and Wei, Luqing and Wendt, Julia and Schreiner, Melinda Westlund and Westlye, Lars T. and Weymar, Mathias and Winkelmann, Tobias and Wu, Guo-Rong and Yoo, Hyun Joo and Quintana, Daniel S.},
  title     = {Cortical thickness and resting-state cardiac function across the lifespan},
  series = {Psychophysiology : journal of the Society for Psychophysiological Research},
  volume    = {58},
  journal   = {Psychophysiology : journal of the Society for Psychophysiological Research},
  number    = {7},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0048-5772},
  doi       = {10.1111/psyp.13688},
  pages     = {16},
  year      = {2020},
  abstract  = {Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting-state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega-analysis (N = 1,218 (50.5\% female), mean age 36.7 years (range: 12-87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS-or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between CT and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research.},
  language  = {en}
}
@article{LiStomaLottaetal.2020,
  author    = {Li, Chen and Stoma, Svetlana and Lotta, Luca A. and Warner, Sophie and Albrecht, Eva and Allione, Alessandra and Arp, Pascal P. and Broer, Linda and Buxton, Jessica L. and Boeing, Heiner and Langenberg, Claudia and Codd, Veryan},
  title     = {Genome-wide association analysis in humans links nucleotide metabolism to leukocyte telomere length},
  series = {American Journal of Human Genetics},
  volume    = {106},
  journal   = {American Journal of Human Genetics},
  number    = {3},
  publisher = {Elsevier},
  address   = {Amsterdam},
  pages     = {16},
  year      = {2020},
  abstract  = {Leukocyte telomere length (LTL) is a heritable biomarker of genomic aging. In this study, we perform a genome-wide meta-analysis of LTL by pooling densely genotyped and imputed association results across large-scale European-descent studies including up to 78,592 individuals. We identify 49 genomic regions at a false dicovery rate (FDR) < 0.05 threshold and prioritize genes at 31, with five highlighting nucleotide metabolism as an important regulator of LTL. We report six genome-wide significant loci in or near SENP7, MOB1B, CARMIL1 , PRRC2A, TERF2, and RFWD3, and our results support recently identified PARP1, POT1, ATM, and MPHOSPH6 loci. Phenome-wide analyses in >350,000 UK Biobank participants suggest that genetically shorter telomere length increases the risk of hypothyroidism and decreases the risk of thyroid cancer, lymphoma, and a range of proliferative conditions. Our results replicate previously reported associations with increased risk of coronary artery disease and lower risk for multiple cancer types. Our findings substantially expand current knowledge on genes that regulate LTL and their impact on human health and disease.},
  language  = {en}
}
@article{LombardoOttenAbdelilahSeyfried2015,
  author    = {Lombardo, Veronica A. and Otten, Cecile and Abdelilah-Seyfried, Salim},
  title     = {Large-scale Zebrafish Embryonic Heart Dissection for Transcriptional Analysis},
  series = {Journal of visualized experiments},
  journal   = {Journal of visualized experiments},
  number    = {95},
  publisher = {JoVE},
  address   = {Cambridge},
  issn      = {1940-087X},
  doi       = {10.3791/52087},
  pages     = {7},
  year      = {2015},
  abstract  = {The zebrafish embryonic heart is composed of only a few hundred cells, representing only a small fraction of the entire embryo. Therefore, to prevent the cardiac transcriptome from being masked by the global embryonic transcriptome, it is necessary to collect sufficient numbers of hearts for further analyses. Furthermore, as zebrafish cardiac development proceeds rapidly, heart collection and RNA extraction methods need to be quick in order to ensure homogeneity of the samples. Here, we present a rapid manual dissection protocol for collecting functional/beating hearts from zebrafish embryos. This is an essential prerequisite for subsequent cardiac-specific RNA extraction to determine cardiac-specific gene expression levels by transcriptome analyses, such as quantitative real-time polymerase chain reaction (RT-qPCR). The method is based on differential adhesive properties of the zebrafish embryonic heart compared with other tissues; this allows for the rapid physical separation of cardiac from extracardiac tissue by a combination of fluidic shear force disruption, stepwise filtration and manual collection of transgenic fluorescently labeled hearts.},
  language  = {en}
}
@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}
}