Laboratory of Genetics of Model Diseases

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About the Laboratory

Metabolic syndrome is defined as the co-occurrence of several risk factors for type 2 diabetes and cardiovascular disease: mainly obesity, insulin resistance, high triglyceride and LDL cholesterol levels, and hypertension. These risk factors are determined by many genes with small effects and their interactions with environmental factors. Genome-wide association studies have so far revealed only a small fraction of the heritability of complex pathophysiological traits in humans. Thus, analyses of animal models of human complex diseases may represent a useful alternative. The department’s research is focused on the following projects:

Uncovering genes regulating hemodynamic and metabolic traits in the SHR strain.
Analysis of the mechanisms underlying the development of salt sensitive hypertension.

Projects

Linkage and correlation analyses of intermediary phenotypes to reveal candidate genes underlying complex pathophysiological traits in the SHR strain

Analysis of the hemodynamic mechanisms of the development of salt sensitive hypertension in hyperaldosteronism

Analysis of the molecular mechanisms underlying hemodynamic abnormalities that initiate the development of hypertension with increased salt intake

Publications

Pravenec; Michal - Mlejnek; Petr - Šimáková; Miroslava - Šilhavý; Jan Hemodynamic Mechanisms Initiating Salt-Sensitive Hypertension in Rat Model of Primary Aldosteronism. Physiological Research. 2024; 73(Suppl.1); S365-S376.

IF = 1.9

de Jong; T. V. - Pan; Y. - Rastas; P. - Munro; D. - Tutaj; M. - Akil; H. - Benner; Ch. - Chen; D. - Chitre; A. S. - Chow; W. - Colonna; V. - Dalgard; C. L. - Demos; W. M. - Doris; P. A. - Garrison; E. - Geurts; A.M. - Gunturkun; H. M. - Guryev; V. - Hourlier; T. - Howe; K. - Huang; J. - Kalbfleisch; T. - Kim; P. - Li; L. - Mahaffej; S. - Martin; F. J. - Mohammadi; P. - Ozel; A. B. - Polesskaya; O. - Pravenec; Michal - Prins; P. - Sebat; J. - Smith; J. R. - Woods; L. C. S. - Tabakoff; B. - Tracey; A. - Uliano-Silva; M. - Villani; F. - Wang; H. - Sharp; B. M. - Telese; F. - Jiang; Z. - Saba; L. - Wang; X. - Murphy; T. D. - Palmer; A. A. - Kwitek; A.E. - Dwinell; M. R. - Williams; R. W. - Li; J. Z. - Chen; H. A revamped rat reference genome improves the discovery of genetic diversity in laboratory rats. Cell Genomics. 2024; 4(4); 100527.

IF = 11.1

Němečková; I. - Eissazadeh; S. - Rathouská Urbánková; J. - Šilhavý; Jan - Malínská; H. - Pravenec; Michal - Nachtigal; P. Transgenic human C-reactive protein affects oxidative stress but not inflammation biomarkers in the aorta of spontaneously hypertensive rats. BMC Cardiovascular Disorders. 2024; 24(1); 211.

IF = 2.0

Čížková; D. - Žurmanová; J.M. - Geryková; L. - Kouvelas; A. - Heleš; M. - Elsnicová; B. - Galatík; F. - Šilhavý; Jan - Pravenec; Michal - Mokrý; J. Nestin expression in intact and hypertrophic myocardium of spontaneously hypertensive rats during aging. Journal of Muscle Research and Cell Motility. 2024; 45(2); 41-51.

IF = 1.8

Šilhavý; Jan - Mlejnek; Petr - Šimáková; Miroslava - Marková; I. - Malínská; H. - Hüttl; M. - Kazdová; L. - Kazantsev; D. - Mancini; M. - Novotný; J. - Pravenec; Michal CD36 regulates substrates utilisation in brown adipose tissue of spontaneously hypertensive rats: In vitro study. PLoS ONE. 2023; 18(4)); e0283276.

IF = 2.9

Kurtz; T. W. - Morris Jr.; R. C. - Pravenec; Michal - Lujan; H. L. - DiCarlo; S. E. Hypertension in Primary Aldosteronism Is Initiated by Salt-Induced Increases in Vascular Resistance With Reductions in Cardiac Output. Hypertension. 2023; 80(5); 1077-1091.

IF = 6.9