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 .