TY  - JOUR
AU  - Tanasković, Slobodan
AU  - Sagić, Dragan Ž.
AU  - Radak, Đorđe J.
AU  - Antonić, Želimir
AU  - Kovačević, Vladimir
AU  - Vuković, Mira
AU  - Aleksić, Nikola
AU  - Radak, Sandra
AU  - Nenezić, Dragoslav
AU  - Cvetković, Slobodan M.
AU  - Isenović, Esma R.
AU  - Vučurević, Goran
AU  - Lozuk, Branko
AU  - Babić, Aleksandar
AU  - Babić, Srđan
AU  - Matić, Predrag
AU  - Gajin, Predrag
AU  - Unić-Stojanović, Dragana
AU  - Ilijevski, Nenad
PY  - 2022
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10259
AB  - Purpose: Carotid artery stenting (CAS) is an option for carotid restenosis (CR) treatment with favorable outcomes. However, CAS has also emerged as an alternative to carotid endarterectomy (CEA) for the management of patients with primary carotid stenosis. This study aimed to report CR rates after CAS was performed in patients with primary lesions versus restenosis after CEA, to identify predictors of CR, and to report both neurological and overall outcomes.Materials and methods:From January 2000 to September 2018, a total of 782 patients were divided into 2 groups: The CAS (prim) group consisted of 440 patients in whom CAS was performed for primary lesions, and the CAS (res) group consisted of 342 patients with CAS due to restenosis after CEA. Indications for CAS were symptomatic stenosis/restenosis >70% and asymptomatic stenosis/restenosis >85%. A color duplex scan (CDS) of carotid arteries was performed 6 months after CAS, after 1 year, and annually afterward. Follow-up ranged from 12 to 88 months, with a mean follow-up of 34.6±18.0 months.Results:There were no differences in terms of CR rate between the patients in the CAS (prim) and CAS (res) groups (8.7% vs 7.2%, ?2=0.691, p=0.406). The overall CR rate was 7.9%, whereas significant CR (>70%) rate needing re-intervention was 5.6%, but there was no difference between patients in the CAS (prim) and CAS (res) groups (6.4% vs 4.7%, p=0.351). Six independent predictors for CR were smoking, associated previous myocardial infarction and angina pectoris, plaque morphology, spasm after CAS, the use of FilterWire or Spider Fx cerebral protection devices, and time after stenting. A carotid restenosis risk index (CRRI) was created based on these predictors and ranged from ?7 (minimal risk) to +10 (maximum risk); patients with a score >?4 were at increased risk for CR. There were no differences in terms of neurological and overall morbidity and mortality between the 2 groups.Conclusions:There was no difference in CR rate after CAS between the patients with primary stenosis and restenosis after CEA. A CRRI score >?4 is a criterion for identifying high-risk patients for post-CAS CR that should be tested in future randomized trials.
T2  - Journal of Endovascular Therapy
T1  - Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index
SP  - 15266028221091895
DO  - 10.1177/15266028221091895
ER  - 

@article{
author = "Tanasković, Slobodan and Sagić, Dragan Ž. and Radak, Đorđe J. and Antonić, Želimir and Kovačević, Vladimir and Vuković, Mira and Aleksić, Nikola and Radak, Sandra and Nenezić, Dragoslav and Cvetković, Slobodan M. and Isenović, Esma R. and Vučurević, Goran and Lozuk, Branko and Babić, Aleksandar and Babić, Srđan and Matić, Predrag and Gajin, Predrag and Unić-Stojanović, Dragana and Ilijevski, Nenad",
year = "2022",
abstract = "Purpose: Carotid artery stenting (CAS) is an option for carotid restenosis (CR) treatment with favorable outcomes. However, CAS has also emerged as an alternative to carotid endarterectomy (CEA) for the management of patients with primary carotid stenosis. This study aimed to report CR rates after CAS was performed in patients with primary lesions versus restenosis after CEA, to identify predictors of CR, and to report both neurological and overall outcomes.Materials and methods:From January 2000 to September 2018, a total of 782 patients were divided into 2 groups: The CAS (prim) group consisted of 440 patients in whom CAS was performed for primary lesions, and the CAS (res) group consisted of 342 patients with CAS due to restenosis after CEA. Indications for CAS were symptomatic stenosis/restenosis >70% and asymptomatic stenosis/restenosis >85%. A color duplex scan (CDS) of carotid arteries was performed 6 months after CAS, after 1 year, and annually afterward. Follow-up ranged from 12 to 88 months, with a mean follow-up of 34.6±18.0 months.Results:There were no differences in terms of CR rate between the patients in the CAS (prim) and CAS (res) groups (8.7% vs 7.2%, ?2=0.691, p=0.406). The overall CR rate was 7.9%, whereas significant CR (>70%) rate needing re-intervention was 5.6%, but there was no difference between patients in the CAS (prim) and CAS (res) groups (6.4% vs 4.7%, p=0.351). Six independent predictors for CR were smoking, associated previous myocardial infarction and angina pectoris, plaque morphology, spasm after CAS, the use of FilterWire or Spider Fx cerebral protection devices, and time after stenting. A carotid restenosis risk index (CRRI) was created based on these predictors and ranged from ?7 (minimal risk) to +10 (maximum risk); patients with a score >?4 were at increased risk for CR. There were no differences in terms of neurological and overall morbidity and mortality between the 2 groups.Conclusions:There was no difference in CR rate after CAS between the patients with primary stenosis and restenosis after CEA. A CRRI score >?4 is a criterion for identifying high-risk patients for post-CAS CR that should be tested in future randomized trials.",
journal = "Journal of Endovascular Therapy",
title = "Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index",
pages = "15266028221091895",
doi = "10.1177/15266028221091895"
}

Tanasković, S., Sagić, D. Ž., Radak, Đ. J., Antonić, Ž., Kovačević, V., Vuković, M., Aleksić, N., Radak, S., Nenezić, D., Cvetković, S. M., Isenović, E. R., Vučurević, G., Lozuk, B., Babić, A., Babić, S., Matić, P., Gajin, P., Unić-Stojanović, D.,& Ilijevski, N.. (2022). Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index. in Journal of Endovascular Therapy, 15266028221091895.
https://doi.org/10.1177/15266028221091895

Tanasković S, Sagić DŽ, Radak ĐJ, Antonić Ž, Kovačević V, Vuković M, Aleksić N, Radak S, Nenezić D, Cvetković SM, Isenović ER, Vučurević G, Lozuk B, Babić A, Babić S, Matić P, Gajin P, Unić-Stojanović D, Ilijevski N. Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index. in Journal of Endovascular Therapy. 2022;:15266028221091895.
doi:10.1177/15266028221091895 .

Tanasković, Slobodan, Sagić, Dragan Ž., Radak, Đorđe J., Antonić, Želimir, Kovačević, Vladimir, Vuković, Mira, Aleksić, Nikola, Radak, Sandra, Nenezić, Dragoslav, Cvetković, Slobodan M., Isenović, Esma R., Vučurević, Goran, Lozuk, Branko, Babić, Aleksandar, Babić, Srđan, Matić, Predrag, Gajin, Predrag, Unić-Stojanović, Dragana, Ilijevski, Nenad, "Carotid Restenosis Rate After Stenting for Primary Lesions Versus Restenosis After Endarterectomy With Creation of Risk Index" in Journal of Endovascular Therapy (2022):15266028221091895,
https://doi.org/10.1177/15266028221091895 . .

TY  - JOUR
AU  - Obradović, Milan M.
AU  - Nikolić, Dragana
AU  - Dobutović, Branislava
AU  - Sudar, Emina
AU  - Soskić, Sanja S.
AU  - Tanasković, Slobodan
AU  - Boljević, Miljana
AU  - Mušicki, Biljana
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10325
AB  - Ateroskleroza se manifestuje kao bolest koronarnih, perifernih i cerebrovaskularnih arterija. Aterosklerotične promene dovode do sužavanja prečnika arterija što dovodi do ishemije u mnogobrojnim organima, čime je poremećeno normalno funkcionisanje kako organa tako i organizma u celini. Centralnu ulogu u patogenezi ateroskleroze zauzima aterogena dislipidemija. Razvoj ateroskleroze počinje malim oštećenjima endotela izazvanim različitim činiocima, koji mogu uticati na povećanje ekspresije adhezivnih molekula. Disfunkcionalni endotel je mesto gde dolazi do infiltracije i akumulacije lipoproteina male gustine (LDL) u vaskularnom zidu. LDL tada podleže oksidativnoj modifikaciji, a kao krajnji produkt nastaje oksidovani LDL (oxLDL). Mnogobrojna eksperimentalna istraživanja ukazuju da su male guste LDL-čestice mnogo aterogenije u poređenju sa većim i lakšim LDL česticama. LDL podleže različitom stepenu oksidacije. Minimalno oksidovani LDL (LDL( - )) pokazuje svoj aterogeni potencijal time što stimuliše vaskularne endotelne ćelije na lučenje velikog broja proinflamatornih molekula kao što su adhezivni molekuli, hemotaktni proteini i faktori rasta. Za razliku od LDL(-), potpuno oksidovani LDL nema sposobnost preuzimanja putem LDL receptora već ga prepoznaju recptori 'hvatači', što dovodi do formiranja makrofag penastih ćelija a u nastavku i stvaranja ateroma. Prisustvo oxLDL u cirkulaciji kod ljudi predstavlja jedan od glavnih faktora rizika od kardiovaskularnih bolesti i ateroskleroze. Buduće studije imaju zadatak da izuče šta se dešava sa oxLDL- om in vivo, kao i da li je i u kojoj meri oksidacija LDL koja igra ključnu ulogu u nastanku penastih ćelija, značajna u kasnijim fazama stvaranja plaka.U okviru ovog preglednog člana, izloženi su najnoviji podaci iz litearture o uticaju oxLDL-a u patogenezi arteroskleroze.
AB  - Atherosclerosis is manifested as a disease of coronary, cerebrovascular and peripheral arteries. Atherosclerotic changes lead to narrowing of the diameter of the arteries leading to ischemia in various organs, which disturbes the normal functioning of both organs and organism as a whole. Atherogenic dyslipidemia has a central role in the pathogenesis of atherosclerosis. Development of atherosclerosis begins with endothelial damage caused by variety of factors, which may cause an increase in expression of adhesion molecules. Dysfunctional endothelium is the place where infiltration and accumulation of low density lipoprotein (LDL) in the vascular wall occurs. LDL undergoes oxidative modification and the final product produced is oxidized LDL (oxLDL). Numerous experimental studies sug- gest that small dense LDL particles are particularly atherogenic compared with larger and lighter LDL particles. LDL is subject to varying degrees of oxidation. Minimally oxidized LDL (LDL(- )) exhibits its atherogenic potential by stimulating vascular endothelial cells to secrete a large number of proinflammatory molecules, such as adhesion molecules, chemotactic proteins, and growth factors. Unlike the LDL(-), fully oxidized LDL cannot bind the LDL receptors, but is recognized by scavenger receptors, which leads to the formation of macrophage foam cells and eventually atheroma. The presence of oxLDL in the circulation in humans is a major risk factor for cardiovascular disease and atherosclerosis. Future studies are warranted to elucidate the role of oxLDL in vivo, and whether and to what extent oxidation of LDL, which plays a key role in the development of foam cells, is critical for later stages in creating the plaque. In this review article, we present current knowledge of the impact of oxLDL in the pathogenesis of arteriosclerosis.
T2  - Medicinska istraživanja
T1  - Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze
T1  - Aterosclerosis and effect of oxidation low density lipoprotein in patogenesis of aterosclerosis
VL  - 45
IS  - 4
SP  - 66
EP  - 71
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10325
ER  - 

@article{
author = "Obradović, Milan M. and Nikolić, Dragana and Dobutović, Branislava and Sudar, Emina and Soskić, Sanja S. and Tanasković, Slobodan and Boljević, Miljana and Mušicki, Biljana and Radak, Đorđe J. and Isenović, Esma R.",
year = "2011",
abstract = "Ateroskleroza se manifestuje kao bolest koronarnih, perifernih i cerebrovaskularnih arterija. Aterosklerotične promene dovode do sužavanja prečnika arterija što dovodi do ishemije u mnogobrojnim organima, čime je poremećeno normalno funkcionisanje kako organa tako i organizma u celini. Centralnu ulogu u patogenezi ateroskleroze zauzima aterogena dislipidemija. Razvoj ateroskleroze počinje malim oštećenjima endotela izazvanim različitim činiocima, koji mogu uticati na povećanje ekspresije adhezivnih molekula. Disfunkcionalni endotel je mesto gde dolazi do infiltracije i akumulacije lipoproteina male gustine (LDL) u vaskularnom zidu. LDL tada podleže oksidativnoj modifikaciji, a kao krajnji produkt nastaje oksidovani LDL (oxLDL). Mnogobrojna eksperimentalna istraživanja ukazuju da su male guste LDL-čestice mnogo aterogenije u poređenju sa većim i lakšim LDL česticama. LDL podleže različitom stepenu oksidacije. Minimalno oksidovani LDL (LDL( - )) pokazuje svoj aterogeni potencijal time što stimuliše vaskularne endotelne ćelije na lučenje velikog broja proinflamatornih molekula kao što su adhezivni molekuli, hemotaktni proteini i faktori rasta. Za razliku od LDL(-), potpuno oksidovani LDL nema sposobnost preuzimanja putem LDL receptora već ga prepoznaju recptori 'hvatači', što dovodi do formiranja makrofag penastih ćelija a u nastavku i stvaranja ateroma. Prisustvo oxLDL u cirkulaciji kod ljudi predstavlja jedan od glavnih faktora rizika od kardiovaskularnih bolesti i ateroskleroze. Buduće studije imaju zadatak da izuče šta se dešava sa oxLDL- om in vivo, kao i da li je i u kojoj meri oksidacija LDL koja igra ključnu ulogu u nastanku penastih ćelija, značajna u kasnijim fazama stvaranja plaka.U okviru ovog preglednog člana, izloženi su najnoviji podaci iz litearture o uticaju oxLDL-a u patogenezi arteroskleroze., Atherosclerosis is manifested as a disease of coronary, cerebrovascular and peripheral arteries. Atherosclerotic changes lead to narrowing of the diameter of the arteries leading to ischemia in various organs, which disturbes the normal functioning of both organs and organism as a whole. Atherogenic dyslipidemia has a central role in the pathogenesis of atherosclerosis. Development of atherosclerosis begins with endothelial damage caused by variety of factors, which may cause an increase in expression of adhesion molecules. Dysfunctional endothelium is the place where infiltration and accumulation of low density lipoprotein (LDL) in the vascular wall occurs. LDL undergoes oxidative modification and the final product produced is oxidized LDL (oxLDL). Numerous experimental studies sug- gest that small dense LDL particles are particularly atherogenic compared with larger and lighter LDL particles. LDL is subject to varying degrees of oxidation. Minimally oxidized LDL (LDL(- )) exhibits its atherogenic potential by stimulating vascular endothelial cells to secrete a large number of proinflammatory molecules, such as adhesion molecules, chemotactic proteins, and growth factors. Unlike the LDL(-), fully oxidized LDL cannot bind the LDL receptors, but is recognized by scavenger receptors, which leads to the formation of macrophage foam cells and eventually atheroma. The presence of oxLDL in the circulation in humans is a major risk factor for cardiovascular disease and atherosclerosis. Future studies are warranted to elucidate the role of oxLDL in vivo, and whether and to what extent oxidation of LDL, which plays a key role in the development of foam cells, is critical for later stages in creating the plaque. In this review article, we present current knowledge of the impact of oxLDL in the pathogenesis of arteriosclerosis.",
journal = "Medicinska istraživanja",
title = "Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze, Aterosclerosis and effect of oxidation low density lipoprotein in patogenesis of aterosclerosis",
volume = "45",
number = "4",
pages = "66-71",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10325"
}

Obradović, M. M., Nikolić, D., Dobutović, B., Sudar, E., Soskić, S. S., Tanasković, S., Boljević, M., Mušicki, B., Radak, Đ. J.,& Isenović, E. R.. (2011). Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze. in Medicinska istraživanja, 45(4), 66-71.
https://hdl.handle.net/21.15107/rcub_vinar_10325

Obradović MM, Nikolić D, Dobutović B, Sudar E, Soskić SS, Tanasković S, Boljević M, Mušicki B, Radak ĐJ, Isenović ER. Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze. in Medicinska istraživanja. 2011;45(4):66-71.
https://hdl.handle.net/21.15107/rcub_vinar_10325 .

Obradović, Milan M., Nikolić, Dragana, Dobutović, Branislava, Sudar, Emina, Soskić, Sanja S., Tanasković, Slobodan, Boljević, Miljana, Mušicki, Biljana, Radak, Đorđe J., Isenović, Esma R., "Ateroskleroza i efekti oksidacije lipoproteina male gustine u patogenezi arteroskleroze" in Medicinska istraživanja, 45, no. 4 (2011):66-71,
https://hdl.handle.net/21.15107/rcub_vinar_10325 .

TY  - JOUR
AU  - Sudar, Emina
AU  - Stokić, Edita
AU  - Nikolić, Dragana
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Obradović, Milan M.
AU  - Tanasković, Slobodan
AU  - Radak, Đorđe J.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/10326
AB  - Sekretagozi hormona rasta (GHS) su sintetička jedinjenja koja su potentni stimulatori oslobađanja hormona rasta (GH) i deluju preko receptora spregnutog sa guanin nukleotid-vezujućim (G) proteinom, koji se naziva GHS-receptor (GHS-R). Metodom reverzne farmakologije identifikovan je i okarakterisan endogeni ligand za GHS-R tipa 1a (GHS-R1a), koji je nazvan grelin. Grelin je peptidni hormon građen od 28 aminokiselina, u kome je aminokiselina Serin-3 (Ser3) noktanoilovana, odnosno ima modifikaciju u vidu lanca masnih kiselina koja je esencijalna za njegovu aktivnost. Grelin se najviše sintetiše u želucu, a GHS-R su eksprimirani većinom u hipotalamusu i hipofizi. Ishrana je najvažniji faktor koji utiče na regulaciju sekrecije grelina. Koncentracija grelina u cirkulaciji povećana je za vreme gladovanja, a opada nakon uzimanja hrane. Grelin stimuliše oslobađanje GH u mnogo većim količinama nego maksimalne doze GH-oslobađajućeg hormona (GHRH) što ukazuje na drugačiji mehanizam delovanja grelina na nivou hipofize. iRNK za grelin i za GHS-R1a identifikovane su i u srcu i u aorti. Proučavanja efekata grelina, pokazala su njegove povoljne efekte na kardiovaskularni sistem (CVS). S obzirom da grelin stimuliše oslobađanje GH, za koji je ranije pokazano da ima kardioprotektivne efekte, grelin može da ispoljava povoljne efekte na CVS posredovane preko GH, ali i efekte koji su nezavisni od efekata GH. Povoljni efekti grelina na CVS pružaju mogućnost da se grelin koristi u terapiji oboljenja CVS kao što su poremećaji u radu srca, hipertenzija i bolesti ishemije srca.
AB  - Small synthetic molecules called growth hormone (GH) secretagogues (GHS) stimulate the release of GH from the pituitary. They act through the GHS-receptor (GHS-R), a G protein coupled receptor. Recently, by using a method of reverse pharmacology the endogenous ligand for the GHS-R type 1a (GHS-R1a) has been discovered. Ghrelin is a 28 amino acid peptide hormone in which the third amino acid serine (Ser3) is modified by a fatty acid and this modification is essential for ghrelin's activity. Ghrelin is produced mainly in the stomach and GHS-R is mainly expressed in hypothalamus and in the pituitary. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone (GHRH), but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. The tissue distribution of ghrelin is widespread, and it is also present in cardiomyocytes. In addition, expression of mRNA encoding both ghrelin and GHSR-1a has been observed in the heart and aortas. Recent evidence indicates that ghrelin feature a variety of cardiovascular activities, including increase of myocardial contractility, vasodilatation, and protection from myocardial infarction. It has been shown that ghrelin may improve cardiac function partly through GH dependent mechanisms but also, some evidence suggests that ghrelin's cardioprotective activity is independent from GH secretion. Thus, ghrelin may be a new therapeutic agent for the treatment of some cardiovascular disturbances and diseases. Further studies are necessary to investigate the potential mechanisms for the effects of ghrelin on cardiovascular system.
T2  - Medicinska istraživanja
T1  - Opšte osobine i efekti grelina na kardiovaskularni sistem
T1  - Ghrelin structure and cardiovascular effects
VL  - 45
IS  - 4
SP  - 15
EP  - 29
UR  - https://hdl.handle.net/21.15107/rcub_vinar_10326
ER  - 

@article{
author = "Sudar, Emina and Stokić, Edita and Nikolić, Dragana and Dobutović, Branislava and Soskić, Sanja S. and Obradović, Milan M. and Tanasković, Slobodan and Radak, Đorđe J. and Isenović, Esma R.",
year = "2011",
abstract = "Sekretagozi hormona rasta (GHS) su sintetička jedinjenja koja su potentni stimulatori oslobađanja hormona rasta (GH) i deluju preko receptora spregnutog sa guanin nukleotid-vezujućim (G) proteinom, koji se naziva GHS-receptor (GHS-R). Metodom reverzne farmakologije identifikovan je i okarakterisan endogeni ligand za GHS-R tipa 1a (GHS-R1a), koji je nazvan grelin. Grelin je peptidni hormon građen od 28 aminokiselina, u kome je aminokiselina Serin-3 (Ser3) noktanoilovana, odnosno ima modifikaciju u vidu lanca masnih kiselina koja je esencijalna za njegovu aktivnost. Grelin se najviše sintetiše u želucu, a GHS-R su eksprimirani većinom u hipotalamusu i hipofizi. Ishrana je najvažniji faktor koji utiče na regulaciju sekrecije grelina. Koncentracija grelina u cirkulaciji povećana je za vreme gladovanja, a opada nakon uzimanja hrane. Grelin stimuliše oslobađanje GH u mnogo većim količinama nego maksimalne doze GH-oslobađajućeg hormona (GHRH) što ukazuje na drugačiji mehanizam delovanja grelina na nivou hipofize. iRNK za grelin i za GHS-R1a identifikovane su i u srcu i u aorti. Proučavanja efekata grelina, pokazala su njegove povoljne efekte na kardiovaskularni sistem (CVS). S obzirom da grelin stimuliše oslobađanje GH, za koji je ranije pokazano da ima kardioprotektivne efekte, grelin može da ispoljava povoljne efekte na CVS posredovane preko GH, ali i efekte koji su nezavisni od efekata GH. Povoljni efekti grelina na CVS pružaju mogućnost da se grelin koristi u terapiji oboljenja CVS kao što su poremećaji u radu srca, hipertenzija i bolesti ishemije srca., Small synthetic molecules called growth hormone (GH) secretagogues (GHS) stimulate the release of GH from the pituitary. They act through the GHS-receptor (GHS-R), a G protein coupled receptor. Recently, by using a method of reverse pharmacology the endogenous ligand for the GHS-R type 1a (GHS-R1a) has been discovered. Ghrelin is a 28 amino acid peptide hormone in which the third amino acid serine (Ser3) is modified by a fatty acid and this modification is essential for ghrelin's activity. Ghrelin is produced mainly in the stomach and GHS-R is mainly expressed in hypothalamus and in the pituitary. The discovery of ghrelin indicates that the release of GH from the pituitary might be regulated not only by hypothalamic GH-releasing hormone (GHRH), but also by ghrelin derived from the stomach. In addition, ghrelin stimulates appetite by acting on the hypothalamic arcuate nucleus, a region known to control food intake. The tissue distribution of ghrelin is widespread, and it is also present in cardiomyocytes. In addition, expression of mRNA encoding both ghrelin and GHSR-1a has been observed in the heart and aortas. Recent evidence indicates that ghrelin feature a variety of cardiovascular activities, including increase of myocardial contractility, vasodilatation, and protection from myocardial infarction. It has been shown that ghrelin may improve cardiac function partly through GH dependent mechanisms but also, some evidence suggests that ghrelin's cardioprotective activity is independent from GH secretion. Thus, ghrelin may be a new therapeutic agent for the treatment of some cardiovascular disturbances and diseases. Further studies are necessary to investigate the potential mechanisms for the effects of ghrelin on cardiovascular system.",
journal = "Medicinska istraživanja",
title = "Opšte osobine i efekti grelina na kardiovaskularni sistem, Ghrelin structure and cardiovascular effects",
volume = "45",
number = "4",
pages = "15-29",
url = "https://hdl.handle.net/21.15107/rcub_vinar_10326"
}

Sudar, E., Stokić, E., Nikolić, D., Dobutović, B., Soskić, S. S., Obradović, M. M., Tanasković, S., Radak, Đ. J.,& Isenović, E. R.. (2011). Opšte osobine i efekti grelina na kardiovaskularni sistem. in Medicinska istraživanja, 45(4), 15-29.
https://hdl.handle.net/21.15107/rcub_vinar_10326

Sudar E, Stokić E, Nikolić D, Dobutović B, Soskić SS, Obradović MM, Tanasković S, Radak ĐJ, Isenović ER. Opšte osobine i efekti grelina na kardiovaskularni sistem. in Medicinska istraživanja. 2011;45(4):15-29.
https://hdl.handle.net/21.15107/rcub_vinar_10326 .

Sudar, Emina, Stokić, Edita, Nikolić, Dragana, Dobutović, Branislava, Soskić, Sanja S., Obradović, Milan M., Tanasković, Slobodan, Radak, Đorđe J., Isenović, Esma R., "Opšte osobine i efekti grelina na kardiovaskularni sistem" in Medicinska istraživanja, 45, no. 4 (2011):15-29,
https://hdl.handle.net/21.15107/rcub_vinar_10326 .