Dalma Kellermayer

ORCID: 0000-0003-0398-0801
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About
Contact & Profiles
Research Areas
  • Cardiomyopathy and Myosin Studies
  • Cardiovascular Effects of Exercise
  • Cardiovascular Function and Risk Factors
  • Cardiovascular and exercise physiology
  • Muscle Physiology and Disorders
  • RNA and protein synthesis mechanisms
  • Renin-Angiotensin System Studies
  • Apelin-related biomedical research
  • Connective tissue disorders research
  • Cardiac Fibrosis and Remodeling
  • Force Microscopy Techniques and Applications
  • Viral Infections and Immunology Research
  • Nitric Oxide and Endothelin Effects
  • Phosphodiesterase function and regulation
  • Nuclear Structure and Function
  • Neurogenetic and Muscular Disorders Research
  • Cardiovascular Disease and Adiposity
  • Molecular Junctions and Nanostructures
  • Heart Failure Treatment and Management
  • Genetics and Physical Performance
  • Systemic Lupus Erythematosus Research
  • Vitamin D Research Studies
  • Nutrition and Health in Aging
  • Cardiac Valve Diseases and Treatments
  • Coenzyme Q10 studies and effects

Semmelweis University
2015-2025

University of Pecs
2023

University of Arizona
2017-2019

Abstract Aims Heart failure with preserved ejection fraction ( HFpEF ) has a great epidemiological burden. The pathophysiological role of cyclic guanosine monophosphate cGMP signalling been intensively investigated in . Elevated levels have shown to exert cardioprotective effects various cardiovascular diseases, including diabetic cardiomyopathy. We the effect long‐term preventive application phosphodiesterase‐ 5A PDE5A inhibitor vardenafil cardiomyopathy‐associated Methods and results...

10.1002/ejhf.711 article EN cc-by-nc-nd European Journal of Heart Failure 2016-12-19

Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide characterization exercise-induced cardiac a rat model using vivo method LV pressure-volume (P-V) analysis. After inducing by swim training, we assessed morphometry...

10.1152/ajpheart.00108.2013 article EN AJP Heart and Circulatory Physiology 2013-05-04

Contractile function is considered to be precisely measurable only by invasive hemodynamics. We aimed correlate strain values measured speckle-tracking echocardiography (STE) with sensitive contractility parameters of pressure-volume (P-V) analysis in a rat model exercise-induced left ventricular (LV) hypertrophy. LV hypertrophy was induced rats swim training and compared untrained controls. Echocardiography performed using 13-MHz linear transducer obtain long- short-axis recordings for STE...

10.1152/ajpheart.00828.2014 article EN AJP Heart and Circulatory Physiology 2015-01-24

Diabetes mellitus (DM) leads to the development of diabetic cardiomyopathy, which is associated with altered nitric oxide (NO)--soluble guanylate cyclase (sGC)--cyclic guanosine monophosphate (cGMP) signalling. Cardioprotective effects elevated intracellular cGMP-levels have been described in different heart diseases. In current study we aimed at investigating pharmacological activation sGC cardiomyopathy.Type-1 DM was induced rats by streptozotocin. Animals were treated either activator...

10.1186/s12933-015-0309-x article EN cc-by Cardiovascular Diabetology 2015-10-31

Marfan syndrome (MFS) is an autosomal dominant disease caused by mutations in the gene (FBN1) of fibrillin-1, a major determinant extracellular matrix (ECM). Functional impairment cardiac left ventricle (LV) these patients usually consequence aortic valve disease. However, LV passive stiffness may also be affected chronic changes mechanical load and ECM dysfunction. Passive determined giant sarcomeric protein titin that has two main splice isoforms: shorter stiffer N2B longer more compliant...

10.1085/jgp.202413690 article EN The Journal of General Physiology 2025-03-10

Left ventricular (LV) hypertrophy is a physiological or pathological response of LV myocardium to increased cardiac load. We aimed at investigating and comparing hemodynamic alterations in well-established rat models (PhyH) (PaH) by using pressure-volume (P-V) analysis. PhyH PaH were induced rats swim training abdominal aortic banding, respectively. Morphology the heart was investigated echocardiography. Characterization function completed P-V In addition, histological molecular biological...

10.1152/ajpheart.00588.2015 article EN AJP Heart and Circulatory Physiology 2015-12-31

Heterozygous (HET) truncating variant mutations in the TTN gene (TTNtvs), encoding giant titin protein, are most common genetic cause of dilated cardiomyopathy (DCM). However, molecular mechanisms by which TTNtv induce DCM controversial. Here, we studied 127 clinically identified human cardiac samples with next-generation sequencing (NGS), high-resolution gel electrophoresis, Western blot analysis, and super-resolution microscopy order to dissect structural functional consequences mutations....

10.1172/jci169753 article EN cc-by Journal of Clinical Investigation 2023-11-14

Although exercise-induced cardiac hypertrophy has been intensively investigated, its development and regression dynamics have not comprehensively described. In the current study, we aimed to characterize effects of regular exercise training detraining on left ventricular (LV) morphology function.Rats were divided into exercised (n = 12) control groups. Exercised rats swam 200 min/day for 12 weeks. After completion protocol, remained sedentary 8 weeks (detraining period). Echocardiographic...

10.1016/j.ijcard.2018.10.092 article EN cc-by-nc-nd International Journal of Cardiology 2018-11-01

Background: Recent evidences suggest that sex hormones may be involved in the regulation of exercise-induced left ventricular (LV) hypertrophy. However, sex-specific functional consequences myocardial hypertrophy is still not investigated detail. We aimed at understanding and morphological alterations LV underlying molecular changes a rat model athlete's heart. Methods: divided our young, adult male female rats into control exercised groups. Athlete's heart was induced by 12-week long swim...

10.3389/fphys.2019.00889 article EN cc-by Frontiers in Physiology 2019-07-12

Abstract Pathologic myocardial hypertrophy develops when the heart is chronically pressure-overloaded. Elevated intracellular cGMP-levels have been reported to prevent development of pathologic hypertrophy, therefore we investigated effects chronic activation cGMP producing enzyme, soluble guanylate cyclase by Cinaciguat in a rat model pressure overload-induced cardiac hypertrophy. Abdominal aortic banding (AAB) was used evoke male Wistar rats. Sham operated animals served as controls....

10.1038/srep37166 article EN cc-by Scientific Reports 2016-11-17

Long-term exercise training is associated with characteristic cardiac adaptation, termed athlete's heart. Our research group previously characterized in vivo left ventricular (LV) function of exercise-induced hypertrophy detail a rat model; however, the effect detraining on LV still unclear. We aimed at evaluating reversibility functional alterations heart after detraining.Rats (n = 16) were divided into detrained exercised (DEx) and control (DCo) groups. Trained rats swam 200 min·d for 12...

10.1249/mss.0000000000001127 article EN Medicine & Science in Sports & Exercise 2016-10-15

Titin is a multifunctional filamentous protein anchored in the M-band, hexagonally organized supramolecular lattice middle of muscle sarcomere. Functionally, M-band framework that cross-links myosin thick filaments, organizes associated proteins, and maintains sarcomeric symmetry via its structural putative mechanical properties. Part appears at C-terminal end isolated titin molecules form globular head, named here "M-complex", which also serves as point head-to-head attachment titin. We...

10.3390/nano12020178 article EN cc-by Nanomaterials 2022-01-06

Long-term exercise induces physiological cardiac adaptation, a condition referred to as athlete's heart. Exercise tolerance is known be associated with decreased passive stiffness. Passive stiffness of the heart muscle determined by giant elastic protein titin. The adult contains two titin isoforms: more compliant N2BA and stiffer N2B. Titin-based may controlled altering expression different isoforms or via post-translational modifications such phosphorylation. Currently, there very limited...

10.3390/ijms222011110 article EN International Journal of Molecular Sciences 2021-10-15

Purpose: Pathological cardiac hypertrophy is observed in pressure overload of the left ventricle. Elevated intracellular cGMP-levels have been reported to prevent development pathological myocardial hypertrophy. We investigated effects chronic activation cGMP producing enzyme, soluble guanylate cyclase (sGC) by cinaciguat a rat model overload-induced Methods: performed aortic banding (AB) evoke our rats. Sham operated animals served as controls. Experimental groups were treated with 10...

10.1093/cvr/cvu091.181 article EN Cardiovascular Research 2014-06-27

Purpose: The role of physical exercise in the prevention and treatment cardiovascular diseases has been well-described, even though elevations cardionecrotic biomarkers after prolonged (i.e. ultramarathon running) were observed. We aimed to establish validate a rat model acute exhaustive determine biochemical, molecular biological, structural functional alterations heart.

10.1093/cvr/cvu098.33 article EN Cardiovascular Research 2014-06-27

Purpose: Long-term exercise training is associated with characteristic structural and functional cardiac adaptation termed athlete's heart. However the effect of discontuniation (detraining) on left ventricular (LV) function still unclear. Our aim was to evaluate development characteristics heart reversibility morphological changes during detraining.

10.1093/cvr/cvu082.17 article EN Cardiovascular Research 2014-06-27

Abstract Heterozygous (HET) truncating mutations in the TTN gene (TTNtv) encoding giant titin protein are most common genetic cause of dilated cardiomyopathy (DCM). However, molecular mechanisms by which TTNtv induce DCM controversial. Here we investigated 127 clinically identified human cardiac samples with next-generation sequencing (NGS), high-resolution gel electrophoresis, Western blot analysis and super-resolution microscopy order to dissect structural functional consequences...

10.1101/2023.02.08.527678 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-02-12
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