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1.

001-es BibID:BIBFORM030249
035-os BibID:WOS:000187895800005
Első szerző:Bányász Tamás (élettanász)
Cím:Profile of I(Ks) during the action potential questions the therapeutic value of I(Ks) blockade / Tamás Bányász, Roland Koncz, László Fülöp, Norbert Szentandrássy, János Magyar, Péter P. Nánási
Dátum:2004
ISSN:0929-8673
Megjegyzések:The goal of this paper is two fold. First, we attempt to review the reports available on the role Of I-Ks in myocardial repolarization. Based on theoretical considerations and experimental results, it seems reasonable to assume that I-Ks blockade will lengthen the action potential. However, results obtained with I-Ks blockers, like chromanol 293B or L-735,821, are conflicting, since from slight lengthening to marked prolongation of action potentials were equally obtained. Although these contradictory results were explained by interspecies or regional differences, the role Of I-Ks in repolarization is a matter of growing dispute. In the second part of this study, we simulated the performance Of I-Ks during cardiac action potentials. We compared the profile of the predicted current in three mathematical models in order to determine the relative role of the current in repolarization. We studied the effect of the cycle length, action potential duration and height of the plateau on the profile Of I-Ks in epicardiac, endocardiac and midmyocardiac ventricular action potentials. The results indicate that the height of the plateau is the most important parameter to control activation Of I-Ks in cardiac tissues, and accordingly, the interspecies and regional differences observed in the efficacy Of I-Ks blockers are likely due to the known differences in action potential morphology. We conclude also that I-Ks blockade may have unpredictable effects on the length of the action potential in a diseased heart, questioning the possible therapeutic value of drugs blocking I-Ks.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 11 : 1 (2004), p. 45-60. -
További szerzők:Koncz Roland Fülöp László (1976-) (kardiológus) Szentandrássy Norbert (1976-) (élettanász) Magyar János (1961-) (élettanász) Nánási Péter Pál (1956-) (élettanász)
Internet cím:DOI
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2.

001-es BibID:BIBFORM020231
035-os BibID:WOS:000294414700009
Első szerző:Bányász Tamás (élettanász)
Cím:Cardiac calmodulin kinase : a potential target for drug design / Banyasz T., Szentandrassy N., Toth A., Nanasi P. P., Magyar J., Chen-Izu Y.
Dátum:2011
ISSN:0929-8673
Megjegyzések:Therapeutic strategy for cardiac arrhythmias has undergone a remarkable change during the last decades. Currently implantable cardioverter defibrillator therapy is considered to be the most effective therapeutic method to treat malignant arrhythmias. Some even argue that there is no room for antiarrhythmic drug therapy in the age of implantable cardioverter defibrillators. However, in clinical practice, antiarrhythmic drug therapies are frequently needed, because implantable cardioverter defibrillators are not effective in certain types of arrhythmias (i.e. premature ventricular beats or atrial fibrillation). Furthermore, given the staggering cost of device therapy, it is economically imperative to develop alternative effective treatments. Cardiac ion channels are the target of a number of current treatment strategies, but therapies based on ion channel blockers only resulted in moderate success. Furthermore, these drugs are associated with an increased risk of proarrhythmia, systemic toxicity, and increased defibrillation threshold. In many cases, certain ion channel blockers were found to increase mortality. Other drug classes such as beta-blockers, angiotensin-converting enzyme inhibitors, aldosterone antagonists, and statins appear to have proven efficacy for reducing cardiac mortality. These facts forced researchers to shift the focus of their research to molecular targets that act upstream of ion channels. One of these potential targets is calcium/calmodulin-dependent kinase II (CaMKII). Several lines of evidence converge to suggest that CaMKII inhibition may provide an effective treatment strategy for heart diseases. (1) Recent studies have elucidated that CaMKII plays a key role in modulating cardiac function and regulating hypertrophy development. (2) CaMKII activity has been found elevated in the failing hearts from human patients and animal models. (3) Inhibition of CaMKII activity has been shown to mitigate hypertrophy, prevent functional remodeling and reduce arrhythmogenic activity. In this review, we will discuss the structural and functional properties of CaMKII, the modes of its activation and the functional consequences of CaMKII activity on ion channels.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3707-3713. -
További szerzők:Szentandrássy Norbert (1976-) (élettanász) Tóth András (farmakológus) Nánási Péter Pál (1956-) (élettanász) Magyar János (1961-) (élettanász) Chen-Izu, Ye
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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3.

001-es BibID:BIBFORM024502
035-os BibID:(WoS)000294414700002 (Scopus)80052005781
Első szerző:Bányász Tamás (élettanász)
Cím:Mechanism of reverse rate-dependent action of cardioactive agents / Tamás Bányász, László Bárándi, Gábor Harmati, László Virág, Norbert Szentandrássy, Ildikó Márton, Antonio Zaza, András Varró, Péter P. Nánási
Dátum:2011
ISSN:0929-8673 1875-533X
Megjegyzések:Class 3 antiarrhythmic agents exhibit reverse rate-dependent lengthening of the action potential duration (APD), i.e. changes in APD are greater at longer than at shorter cycle lengths. In spite of the several theories developed to explain this reverse rate-dependency, its mechanism has been clarified only recently. The aim of the present study is to elucidate the mechanisms responsible for reverse rate-dependency in mammalian ventricular myocardium. Action potentials were recorded using conventional sharp microelectrodes from human, canine, rabbit, guinea pig, and rat ventricular myocardium in a rate-dependent manner. Rate-dependent drug-effects of various origin were studied using agents known to lengthen or shorten action potentials allowing thus to determine the drug-induced changes in APD as a function of the cycle length. Both drug-induced lengthening and shortening of action potentials displayed reverse rate-dependency in human, canine, and guinea pig preparations, but not in rabbit and rat myocardium. Similar results were obtained when repolarization was modified by injection of inward or outward current pulses in isolated canine cardiomyocytes. In contrast to reverse rate-dependence, drug-induced changes in APD well correlated with baseline APD values (i.e. that measured before the superfusion of drug or injection of current) in all of the preparations studied. Since the net membrane current (I(net)), determined from the action potential waveform at the middle of the plateau, was inversely proportional to APD, and consequently to cycle length, it is concluded that that reverse rate-dependency may simply reflect the inverse relationship linking I(net) to APD. In summary, reverse rate-dependency is an intrinsic property of drug action in the hearts of species showing positive APD - cycle length relationship, including humans. This implies that development of a pure K(+) channel blocking agent without reverse rate-dependent effects is not likely to be successful.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
antiarrhythmiás szerek
APD
Molekuláris Medicina
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current medicinal chemistry. - 18 : 24 (2011), p. 3597-3606. -
További szerzők:Bárándi László (1984-) (élettanász) Harmati Gábor (1983-) (élettanász) Virág László (élettanász Szeged) Szentandrássy Norbert (1976-) (élettanász) Márton Ildikó (1954-) (fogszakorvos) Zaza, Antonio Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
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4.

001-es BibID:BIBFORM059983
Első szerző:Docsa Tibor (vegyész, biokémikus)
Cím:Insulin sensitivity is modified by a glycogen phosphorylase inhibitor : glucopyranosylidene-spiro-thiohydantoin in streptozotocin-induced diabetic rats / Tibor Docsa, Balázs Marics, József Németh, Csaba Hüse, László Somsák, Pál Gergely, Barna Peitl
Dátum:2015
ISSN:1568-0266
Megjegyzések:The major role of liver glycogen is to supply glucose to the circulation maintaining the normal blood glucose level. In muscle and liver the accumulation and breakdown of glycogen are regulated by the reciprocal activities of glycogen phosphorylase and glycogen synthase. Glycogen phosphorylase catalyses the key step of glycogen degradation and its activity can be inhibited by glucose and its analogues. Obviously, any readily accessible inhibitor of glycogen phosphorylase can be used as a potential therapy of non-insulin-dependent or type 2 diabetes. Hepatic glycogen phosphorylase has been identified as a new target for drugs that control blood glucose concentration. In our experiments glucopyranosylidene-spirothiohydantoin (TH) was tested on the insulin sensitivity and blood glucose level of control and streptozotocin-treated rats. The streptozotocin-treated rats failed to gain weight and exhibited stable hyperglycemia (4.7 ± 0.5 mmol/L glucose in control vs. 7.8 ± 0.5 mmol/L) and low plasma insulin levels (9.6 ± 1.9 [mű]IU/mL in control vs. 3.2 ± 2.2 [mű]IU/mL). When insulin supplementation with slow-release implants (2 IU/day) was started 8 weeks after streptozotocin injection, blood glucose concentration remained suppressed, plasma insulin level dramatically increased and the insulin sensitivity restored. TH administration significantly reduced the high blood glucose concentration and restored the insulin sensitivity of STZtreated rats.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Blood glucose
glycogen phosphorylase inhibitor
insulin implant
streptozotocin
Type 2 diabetes
Megjelenés:Current Topics In Medicinal Chemistry 15 : 23 (2015), p. 2390-2394. -
További szerzők:Marics Balázs (1986-) (okleveles táplálkozástudományi szakember, dietetikus) Németh József (1954-) (vegyész, analitikus) Hüse Csaba Somsák László (1954-) (vegyész) Gergely Pál (1947-) (biokémikus) Peitl Barna (1972-) (orvos, farmakológus)
Pályázati támogatás:OTKA-109450
OTKA
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5.

001-es BibID:BIBFORM049492
Első szerző:Hegyi Bence (élettanász)
Cím:Selectivity problems with drugs acting on cardiac Na+ and Ca2+ channels / Bence Hegyi, István Komáromi, Péter P. Nánási, Norbert Szentandrássy
Dátum:2013
ISSN:0929-8673
Megjegyzések:With the increase of our knowledge on cardioactive agents it comes more and more clear that practically none of the currently used compounds shows absolute selectivity to one or another ion channel type. This is particularly true for Na(+) and Ca(2+) channel modulators, which are widely applied in the clinical practice and biomedical research. The best example might be probably the marine guanidine poison tetrodotoxin, which has long been considered as a selective Na(+) channel blocker, while recently it turned out to effectively inhibit cardiac Ca(2+) currents as well. In the present study the cross actions observed between the effects of various blockers of Na(+) channels (such as toxin inhibitors, class I antiarrhythmics and local anesthetics) and Ca(2+) channels (like phenylalkylamines, dihydropyridine compounds, diltiazem and mibefradil) are overviewed in light of the known details of the respective channel structures. Similarly, activators of Na(+) channels, including veratridine and batrachotoxin, are also compared. The binding of tetrodotoxin and saxitoxin to Cav1.2 and Nav1.5 channel proteins is presented by construction of theoretical models to reveal common structures in their pore forming regions to explain cross reactions. Since these four domain channels can be traced back to a common ancestor, a close similarity in their structure can well be demonstrated. Thus, the poor selectivity of agents acting on cardiac Na(+) and Ca(2+) channels is a consequence of evolution. As a conclusion, since the limited selectivity is an intrinsic property of drug receptors, it has to be taken into account when designing new cardioactive compounds for either medical therapy or experimental research in the future.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Na+ channels
Ca2+ channels
ion selectivity
cardioactive drugs
channel structures
tetrodotoxin
Doktori iskola
Megjelenés:Current Medicinal Chemistry. - 20 : 20 (2013), p. 2552-2571. -
További szerzők:Komáromi István (1957-) (vegyész, molekuláris biológus, biokémikus) Nánási Péter Pál (1956-) (élettanász) Szentandrássy Norbert (1976-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.2.A-11/1/KONV-2012-0045
TÁMOP
Élettan Kutatócsoport
K100151
OTKA
PD101171
OTKA
K101196
OTKA
CNK-77855
OTKA
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Orvostudomány Doktori Iskola
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DOI
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6.

001-es BibID:BIBFORM001935
Első szerző:Kappelmayer János (laboratóriumi szakorvos)
Cím:Pgp and FLT3 : identification and modulation of two proteins that lead to chemotherapy resistance in acute myeloid leukemia / Kappelmayer János, Udvardy Miklós, Antal-Szalmás Péter
Dátum:2007
Megjegyzések:Acute myeloid leukaemia (AML) comprises 80% of acute adult leukaemias and the disease has mostly an unfavourable outcome. Diagnostic criteria rely primarily on morphological classification, while prognostic evaluation is determined by cytogenetic methods. Survival is highly variable and it is a matter of debate, whether alternative therapeutic approaches may improve the effectiveness of conventional cytotoxic drug treatment. Two transmembrane proteins undoubtedly contribute to worse prognosis: P-glycoprotein (Pgp) and FLT3. Pgp is a transmembrane, ATP-cassette binding efflux pump that efficiently removes structurally unrelated xenobiotics from leukaemic blasts. This leads to inefficiency towards several cytotoxic drugs, hence the phenomenon is called multidrug resistance. FLT3 is a transmembrane tyrosine kinase and an internal tandem duplication can considerably augment its kinase activity. Both mechanisms lead to chemotherapy resistance and significantly shorter survival; thus several studies have been designed to treat patients via therapeutic measures that neutralize these proteins. This review focuses on the pathophysiological phenomena and the detection methods of Pgp and FLT3 as well as on novel therapeutic strategies that are offered by their inhibition.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
acute myeloid leukaemia
p-glycoprotein
FLT-3 mutation
Megjelenés:Current Medical Chemistry. - 14 : 5 (2007), p. 519-530. -
További szerzők:Udvardy Miklós (1947-) (belgyógyász, haematológus) Antal-Szalmás Péter (1968-) (laboratóriumi szakorvos)
Internet cím:elektronikus változat
Borító:

7.

001-es BibID:BIBFORM047105
035-os BibID:PMID:23244521
Első szerző:Kovács András László (biológus, biológia-kémia tanár)
Cím:Medicinal chemistry meets proteomics : fractionation of the human plasma proteome / András Kovács, András Guttman
Dátum:2013
ISSN:0929-8673
Megjegyzések:Human plasma and its fractions/derivatives are frequently used materials in biomedicine as it contains thousands and thousands of proteins representing the majority of human proteome. Several important methods were developed in the past for the fractionation of this important biological fluid and its use for medicinal purposes. One of the greatest challenges is the very large dynamic range of plasma proteins ranging up to 10-12 orders of magnitude. Early attempts were mainly based on methods such as salting out or cold ethanol precipitation, as well as chromatography utilizing affinity, size exclusion, ion exchange and hydrophobic interaction techniques. More recently, fractionation applications started with the depletion of the high abundant plasma components, such as serum albumin and immunoglobulins, before isolating lower abundant proteins of interest. Plasma volumes were utilized from the milliliter scale for diagnostic applications to hundreds of liters for industrial scale plasma fractionation (e.g., medicinal product manufacturing). In this paper we review this important part of medicinal chemistry, highlighting the traditional methods along with some of their variations as well as the most significant recent achievements of the field.
Tárgyszavak:Természettudományok Kémiai tudományok idegen nyelvű folyóiratközlemény külföldi lapban
Doktori iskola
Megjelenés:Current Medicinal Chemistry. - 20 : 4 (2013), p. 483-490. -
További szerzők:Guttman András (1954-) (vegyészmérnök)
Pályázati támogatás:K-81839 OTKA
OTKA
TÁMOP-4.2.2/B-10/1-2010-0024
TÁMOP
Molekuláris Orvostudomány Doktori Iskola
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DOI
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8.

001-es BibID:BIBFORM020232
035-os BibID:WOS:000294414700010
Első szerző:Magyar János (élettanász)
Cím:Long term regulation of cardiac L-type calcium channel by small G proteins / Magyar J., Jenes A., Kistamas K., Ruzsnavszky F., Nanasi P. P., Satin J., Szentandrassy N., Banyasz T.
Dátum:2011
ISSN:0929-8673
Megjegyzések:Calcium ions are crucial elements of excitation-contraction coupling in cardiac myocytes. The intracellular Ca(2+) concentration changes continously during the cardiac cycle, but the Ca(2+) entering to the cell serves as an intracellular second messenger, as well. The Ca(2+) as a second messenger influences the activity of many intracellular signalling pathways and regulates gene expression. In cardiac myocytes the major pathway for Ca(2+) entry into cells is L-type calcium channel (LTCC). The precise control of LTCC function is essential for maintaining the calcium homeostasis of cardiac myocytes. Dysregulation of LTCC may result in different diseases like cardiac hypertrophy, arrhytmias, heart failure. The physiological and pathological structural changes in the heart are induced in part by small G proteins. These proteins are involved in wide spectrum of cell biological functions including protein transport, regulation of cell proliferation, migration, apoptosis, and cytoskeletal rearrangement. Understanding the crosstalk between small G proteins and LTCC may help to understand the pathomechanism of different cardiac diseases and to develop a new generation of genetically-encoded Ca(2+) channel inhibitors.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3714-3719. -
További szerzők:Jenes Ágnes (1980-) (élettanász) Kistamás Kornél (1986-) (biológus) Ruzsnavszky Ferenc (1984-) (élettanász) Nánási Péter Pál (1956-) (élettanász) Satin, Jonathan Szentandrássy Norbert (1976-) (élettanász) Bányász Tamás (1960-) (élettanász)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
A feszültségfüggő K-csatornák szerepe excitábilis sejtekben
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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9.

001-es BibID:BIBFORM028396
Első szerző:Nagy Béla Jr. (labordiagnosztikai szakorvos)
Cím:Potential therapeutic targeting of platelet-mediated cellular interactions in atherosclerosis and inflammation / B. Nagy Jr., K. Miszti-Blasius, A. Kerényi, K. J. Clemetson, J. Kappelmayer
Dátum:2012
ISSN:0929-8673
Megjegyzések:Cellular interactions among platelets, leukocytes and endothelial cells are considered as a major cause of inflammation and atherosclerosis in many diseases. Via exposed surface receptors and released soluble substances, activated platelets play a crucial role in the initiation of inflammatory processes, resulting in endothelial injury and leading to formation of atherosclerotic plaque with possible thrombotic complications. Classic anti-platelet treatments (e.g. cyclooxygenase inhibitor or ADP-receptor antagonist) have favorable effects in patients with vascular diseases, but they also have several limitations such as increased bleeding risk or non-responsiveness. Thus, the need and opportunities for developing novel therapeutic inhibitors for platelet-mediated events are obvious. Animal and (pre)clinical human studies have suggested that some recently produced specific antagonists of P-selectin from α-granules, as well as its main ligand/receptor P-selectin Glycoprotein Ligand-1, the two major platelet chemokines CXCL4 and CCL5, as well as CD40L, may be considered potential new candidates in the treatment of atherogenesis and inflammation. In this review, we summarize the pathophysiological roles of these effectors in platelet activation and acute or chronic inflammation, and discuss the latest findings on promising antagonistic agents in basic and clinical studies in the prevention of platelet-mediated cellular interaction.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Molekuláris Medicina
atherosclerosis
CD40L
chemokine
endothelial cell
inflammation
leukocyte
platelet
P-selectin
Megjelenés:Current Medicinal Chemistry. - 19 : 4 (2012), p. 518-531. -
További szerzők:Miszti-Blasius Kornél (1977-) (laboratóriumi szakorvos) Kerényi Adrienne (1970-) (laboratóriumi szakorvos) Clemetson, Kenneth J. Kappelmayer János (1960-) (laboratóriumi szakorvos)
Pályázati támogatás:TÁMOP-4.2.1/B-09/1/KONV-2010-0007
TÁMOP
Celluláris hematológia - immunológia
OTKA T75199
OTKA
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10.

001-es BibID:BIBFORM020356
Első szerző:Nagy N. (Szeged)
Cím:Role of Ca(2)+-sensitive K+ currents in controlling ventricular repolarization : possible implications for future antiarrhytmic drug therapy / Nagy N., Marton Z., Kiss L., Varro A., Nanasi P. P., Toth A.
Dátum:2011
ISSN:1875-533X (Electronic)
Megjegyzések:Normal heart function and repolarization of the cardiac action potential (AP) is to a high extent subjective to synchronized activity of sarcolemmal K(+) channels, expressed in both ventricular and atrial myocardium, largely contributing to regulation of the resting potential, the pacemaker activity, and the shape and duration of the AP. Clinical observations and experimental studies in cardiomyocytes and multicellular preparations provided firm evidence for the sensitivity of some major outward K+ currents and the corresponding ion channels to shifts in intracellular Ca(2+) concentration ([Ca(2+)](i)). Direct regulation via interaction between [Ca(2+ )](i) and the channel protein or indirect modulation via Ca(2+ ) signaling pathways of these currents have strong implications to mechanical and electrical performance of the heart, and its physiological adaptation to altered load. It may also lead to severe cardiac dysfunction, if [Ca(2+ )](i) handling is disturbed in a variety of pathological conditions. In this review we attempt to summarize the present state of the topic on two ubiquitous repolarizing K(+) currents (I(to1) and I(K1)) with documented Ca(2+)-sensitivity and critical significance in cellular antiarrhythmic defense, to highlight fields where clue data are missing, and discuss the apparently unsolved "mystery" of the cardiac small conductance Ca(2+ )-activated K(+ ) (SK) channels. We have collected the available information on the known novel, although usually still not enough selective inhibitors and activators of these currents justifying the need for more selective ones. Finally, we emphasize a few related therapeutical perspectives to be considered for future experimental research and particularly in pharmaceutical development.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3622-3639. -
További szerzők:Marton Z. Kiss L. Varró András (1954-) (farmakológus, klinikai farmakológus) Nánási Péter Pál (1956-) (élettanász) Tóth András (farmakológus)
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11.

001-es BibID:BIBFORM077899
035-os BibID:(PMID)29278207 (WoS)000432247500002 (Scopus)85048878557
Első szerző:Nánási Péter Pál ifj. (sejtbiológus)
Cím:Omecamtiv Mecarbil : a Myosin Motor Activator Agent with Promising Clinical Performance and New in vitro Results / Péter Nánási Jr., István Komáromi, Marta Gaburjakova, János Almássy
Dátum:2018
ISSN:0929-8673
Megjegyzések:Abstract: Background: Clinical treatment of heart failure is still suffering from limited efficacy and unfavorable side effects. The recently developed group of agents, the myosin motor activators, act directly on cardiac myosin resulting in an increased force generation and prolongation of contraction. The lead molecule, omecamtiv mecarbil is now in human 3 stage. In addition tothe promising clinical data published so far, there are new in vitro results indicating that the effect of omecamtiv mecarbil on contractility is rate-dependent. Furthermore, omecamtiv mecarbilwas shown to activate cardiac ryanodine receptors, an effect that may carry proarrhythmic risk. Methods: These new results, together with the controversial effects of the drug on cardiac oxygen consumption, are critically discussed in this review in light of the current literature on omecamtiv mecarbil. Results: In therapeutically relevant concentrations the beneficial inotropic effect of the agent isnot likely affected by these new results - in accordance with the good clinical data. At supratherapeutic concentrations, however, activation of cardiac ryanodine receptors may increasearrhythmia propensity, and the stronger effect on diastolic than systolic cell shortening, observed at higher pacing frequencies, may decrease or offset the inotropic effect of omecamtivmecarbil. Conclusion: Further studies with definitely supratherapeutical concentrations of omecamtivmecarbil should be designed to map the actual risk of these potentially harmful side-effects.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Heart failure
inotropic agents
myosin activators
Omecamtiv mecarbil
Ryanodine receptor
Cytosolic Ca 2+
Megjelenés:Current Medicinal Chemistry. - 25 : 15 (2018), p. 1720-1728. -
További szerzők:Komáromi István (1957-) (vegyész, molekuláris biológus, biokémikus) Gaburjakova, Marta Almássy János (1981-) (élettanász, biológus, angol-magyar szakfordító)
Pályázati támogatás:NKFIH PD112199
NKFIH
Janos Bolyai Research Scholarship of the Hungarian Academy of Sciences
MTA
Szodoray Scholarship of the University of Debrecen
Egyéb
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DOI
Intézményi repozitóriumban (DEA) tárolt változat
Borító:

12.

001-es BibID:BIBFORM030213
035-os BibID:(WOS)000294414700001
Első szerző:Nánási Péter Pál (élettanász)
Cím:Hot topic : hot topics in cellular cardiac electrophysiology with potential impact on future drug design / Péter P. Nánási, Valéria Kecskeméti
Dátum:2011
ISSN:0929-8673
Tárgyszavak:Orvostudományok Elméleti orvostudományok szerkesztőségi anyag
folyóiratcikk
egyetemen (Magyarországon) készült közlemény
Megjelenés:Current Medicinal Chemistry. - 18 : 24 (2011), p. 3595-3596. -
További szerzők:Kecskeméti Valéria
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
Borító:
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