Robert Halmosi

Prof. Dr. Robert Halmosi

orcid

Research Focus & Metrics

Academic Career Length

28Years (1999-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2012 in Clinical Hemorheology and Microcirculation
Verified
Journal Article
Closed access
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KMK. Magyar
K. Magyar
RHRobert Halmosi
Robert Halmosi
APA. Palfi
A. Palfi
Gergely FeherGergely Feher
Gergely Feher
LCL. Czopf
L. Czopf
Eszter SzabadosEszter Szabados
Eszter Szabados
Several beneficial effects of resveratrol (RES), a natural antioxidant present in red wine have already been described. The aim of our study was to investigate if RES had a clinically measurable cardioprotective effect in patients after myocardial in

1 June 2018 in JACC: Heart Failure
Verified
Journal Article
Closed access
MCMarco Canepa
Marco Canepa
CFCandida Fonseca
Candida Fonseca
OCOvidiu Chioncel
Ovidiu Chioncel
CLCécile Laroche
Cécile Laroche
MCMaria G. Crespo-Leiro
Maria G. Crespo-Leiro
HGH. Gunes
H. Gunes

1 June 2001 in Molecular Pharmacology
Verified
Journal Article
Closed access
RHRobert Halmosi
Robert Halmosi
ZBZoltan Berente
Zoltan Berente
EOErzsebet Osz
Erzsebet Osz
KTKalman Toth
Kalman Toth
PLPeter Literati-Nagy
Peter Literati-Nagy
BSBalazs Sumegi
Balazs Sumegi
Ischemia-reperfusion induces reactive oxygen species (ROS) formation, and ROS lead to cardiac dysfunction, in part, via the activation of the nuclear poly(ADP-ribose) polymerase (PARP, called also PARS and ADP-RT). ROS and peroxynitrite induce single-strand DNA break formation and PARP activation, resulting in NAD+ and ATP depletion, which can lead to cell death. Although protection of cardiac muscle by PARP inhibitors can be explained by their attenuating effect on NAD+ and ATP depletion, there are data indicating that PARP inhibitors also protect mitochondria from oxidant-induced injury. Studying cardiac energy metabolism in Langendorff heart perfusion system by 31P NMR, we found that PARP inhibitors (3-aminobenzamide, nicotinamide, BGP-15, and 4-hydroxyquinazoline) improved the recovery of high-energy phosphates (ATP, creatine phosphate) and accelerated the reutilization of inorganic phosphate formed during the ischemic period, showing that PARP inhibitors facilitate the faster and more complete recovery of the energy production. Furthermore, PARP inhibitors significantly decrease the ischemia-reperfusion-induced increase of lipid peroxidation, protein oxidation, single-strand DNA breaks, and the inactivation of respiratory complexes, which indicate a decreased mitochondrial ROS production in the reperfusion period. Surprisingly, PARP inhibitors, but not the chemically similar 3-aminobenzoic acid, prevented the H2O2-induced inactivation of cytochrome oxidase in isolated heart mitochondria, suggesting the presence of an additional mitochondrial target for PARP inhibitors. Therefore, PARP inhibitors, in addition to their important primary effect of decreasing the activity of nuclear PARP and decreasing NAD+ and ATP consumption, reduce ischemia-reperfusion-induced endogenous ROS production and protect the respiratory complexes from ROS induced inactivation, providing an additional mechanism by which they can protect heart from oxidative damages.

1 January 2017 in Oxidative Medicine and Cellular Longevity
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Journal Article
Open access
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ÁRÁdám Riba
Ádám Riba
LDLaszlo Deres
Laszlo Deres
BSBalazs Sumegi
Balazs Sumegi
KTKalman Toth
Kalman Toth
Eszter SzabadosEszter Szabados
Eszter Szabados
RHRobert Halmosi
Robert Halmosi
Despite great advances in therapies observed during the last decades, heart failure (HF) remained a major health problem in western countries. In order to further improve symptoms and survival in patients with heart failure, novel therapeutic strategies are needed. In some animal models of HF resveratrol (RES), it was able to prevent cardiac hypertrophy, contractile dysfunction, and remodeling. Several molecular mechanisms are thought to be involved in its protective effects, such as inhibition of prohypertrophic signaling molecules, improvement of myocardial Ca2+ handling, regulation of autophagy, and the reduction of oxidative stress and inflammation. In our present study, we wished to further examine the effects of RES on prosurvival (Akt‐1, GSK‐3β) and stress signaling (p38‐MAPK, ERK 1/2, and MKP‐1) pathways, on oxidative stress (iNOS, COX‐2 activity, and ROS formation), and ultimately on left ventricular function, hypertrophy and fibrosis in a murine, and isoproterenol‐ (ISO‐) induced postinfarction heart failure model. RES treatment improved left ventricle function, decreased interstitial fibrosis, cardiac hypertrophy, and the level of plasma BNP induced by ISO treatment. ISO also increased the activation of P38‐MAPK, ERK1/2Thr183-Tyr185, COX‐2, iNOS, and ROS formation and decreased the phosphorylation of Akt‐1, GSK‐3β, and MKP‐1, which were favorably influenced by RES. According to our results, regulation of these pathways may also contribute to the beneficial effects of RES in HF.

Verified
Journal Article
Open access
PDF file
RGRoland Gal
Roland Gal
LDLaszlo Deres
Laszlo Deres
KTKalman Toth
Kalman Toth
RHRobert Halmosi
Robert Halmosi
THTamas Habon
Tamas Habon
Cardiovascular diseases are the leading causes of death worldwide. The cardioprotective effects of natural polyphenols such as resveratrol (3,5,4-trihydroxystilbene) have been extensively investigated throughout recent decades. Many studies of RES have focused on its favorable effects on pathological conditions related to cardiovascular diseases and their risk factors. The aim of this review was to summarize the wide beneficial effects of resveratrol on the cardiovascular system, including signal transduction pathways of cell longevity, energy metabolism of cardiomyocytes or cardiac remodeling, and its anti-inflammatory and antioxidant properties. In addition, this paper discusses the significant preclinical and human clinical trials of recent years with resveratrol on cardiovascular system. Finally, we present a short overview of antiviral and anti-inflammatory properties and possible future perspectives on RES against COVID-19 in cardiovascular diseases.

1 January 2002 in Clinical Neuropharmacology
Verified
Journal Article
Closed access
BHBeata Horvath
Beata Horvath
ZMZsolt Marton
Zsolt Marton
RHRobert Halmosi
Robert Halmosi
TATamas Alexy
Tamas Alexy
LSLaszlo Szapary
Laszlo Szapary
KTKalman Toth
Kalman Toth
Oxygen-free radicals play an important role in several physiologic and pathophysiologic processes. In pathologic circumstances, they can modify and damage biologic systems. Because oxygen-free radicals are involved in a wide range of diseases (cerebrovascular, cardiovascular, etc.), scavenging these radicals should be considered as an important therapeutic approach. In our in vitro study, we investigated the antioxidant capacity of three drugs: pentoxiphylline (Sigma Aldrich, St. Louis, MO, USA) piracetam (Sigma Aldrich), and vinpocetine (Richter Gedeon RT, Budapest, Hungary). Phenazine methosulphate was applied to generate free radicals, increasing red blood cell rigidity. Filtration technique and potassium leaking were used to detect the cellular damage and the scavenging effect of the examined drugs. According to our results, at human therapeutic serum concentration, only vinpocetine (Richter Gedeon RT) had significant (p < 0.01) scavenging activity with a protective effect that increased further at higher concentrations. Pentoxiphylline (Sigma Aldrich) and piracetam (Sigma Aldrich) did not have significant antioxidant capacity at therapeutic concentrations, but increasing their concentrations (pentoxiphylline at 100-times, and piracetam at 10-times higher concentrations) led to a significant (p < 0.01) scavenger effect. Our findings suggest that this pronounced antioxidant effect of vinpocetine and even the milder scavenging capacity of pentoxiphylline and piracetam may be of value in the treatment of patients with cerebrovascular disorders, but merits further investigations.