ZNAČAJ ZAPALJENSKOG PROCESA U PATOGENEZI, DIJAGNOZI I TERAPIJI ATEROSKLEROZE
Sažetak
Ateroskleroza je hronična bolest čija progresija kreće od rođenja. Osnovni supstrat aterosklerotske lezije je deponovanje lipida u intimu krvnog suda, što ima za rezultat postupno suženje i otežan protok krvi kroz tkiva. Kliničke manifestacije aterosklerotskog procesa su brojne i one zavise od stepena suženja i brzine nastanka stenoze. Kliničke manifestacije koje su najčešće predstavljaju posledicu rupture aterosklerotskog plaka što aktivira proces trombogeneze i dovodi do razvoja začepljenja krvnih sudova. Najznačajniji faktori rizika za aterosklerozu su povišeni LDL, smanjeni HDL, upotreba cigareta, hipertenzija, tip II diabetes mellitus, starost, porodična anamneza koja se vezuje za kardiovaskularne bolesti kod rođaka u prvoj liniji (muškarci mlađi od 55 godina, žene mlađe od 65 godina). Kada se posmatraju blagi oblici ateroskleroze, uglavnom nemaju nikakve simptome. A kod uznapredovale ateroskleroze javljaju se vidljivi i osetni simptomi koji variraju u zavisnosti od toga koju arteriju zahvata. Neki od njih su: bol u grudima – izaziva ga ateroskleroza u srčanim arterijama, akutna ishemija mozga ili šlog – izaziva ih ateroskleroza u arterijama koje vode do mozga, poteškoće sa hodanjem – sužene arterije u nogama, povišen krvni pritisak, zatajenje bubrega, erektilna disfunkcija kod muškaraca i bolni odnosi kod žena – ateroskleroza u arterijama genitalnog trakta. Cilj ovog rada jeste adekvatno istražiti i prikazati vezu između inflamacije i ateroskleroze.
Reference
2. Wilcox J, Smith K, Schwatrz S, Gordon D. Localization of tissue factor in the normal vessel wall and in the atherosclerotic plaque. Proc Natl Acad Sci USA. 1989; 86: 2839 – 2843.
3. Ross R, Glomset J. Atherosclerosis and the arterial smooth muscle cell: proliferation of smooth muscle is a key event in the genesis of the lesions of atherosclerosis. Science. 1973; 180: 1332 – 1339.
4. Williams K, Tabas I. The response-to-retention hypothesis of early atherosclerosis. Arterioscl Thromb Vasc Biol. 1995; 15: 551 – 561.
5. Williams K, Tabas I. The response-to-retention hypothesis of atherosclerosis reinforced. Curr Opin Lipidol. 1998; 9: 471 – 474.
6. Goldstein J, Ho Y, Basu S, Brown M. Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition. Proc Natl Acad Sci USA. 1979; 76: 333 -337.
7. Tabas I. Macrophage death and defective inflammation resolution in atherosclerosis. Nat. Rev. Immunol. 2010; 10:36–46. doi: 10.1038/nri2675.
8. Calabro P, Willerson J.T, Yeh E.T. Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells. Circulation, 2003; 108: 1930-1932.
9. Björkegren JLM, Lusis AJ. Atherosclerosis: Recent developments. Cell. 2022 May 12;185(10):1630-1645. doi: 10.1016/j.cell.2022.04.004.
10. Pasceri V, Chang J, Willerson JT, et al. Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs. Circulation. 2001; 103: 2531–2534.
11. Ross R. Atherosclerosis--an inflammatory disease. N Engl J Med. 1999 Jan 14;340(2):115-26. doi: 10.1056/NEJM199901143400207
12. Ridker P.M. Clinical application of C-reactive protein for cardiovascular disease detection and prevention. Circulation, 2003; 107: 363-369.
13. Barbu E; Popescu MR, Popescu AC, Balanescu SM. Inflammation as A Precursor of Atherothrombosis, Diabetes and Early Vascular Aging. Int. J. Mol. Sci. 2022, 23, 963. https://doi.org /10.3390/ijms23020963
14. Witztum JL, Berliner JA. Oxidized phospholipids and isoprostanes in atherosclerosis. Curr Opin Lipidol. 1998; 9: 441–448.
15. Kotlyarov S.; Kotlyarova A.Involvement of Fatty Acids and Their Metabolites in the Development of Inflammation in Atherosclerosis. Int. J. Mol. Sci. 2022, 23, 1308. https://doi.org/10.3390/ijms23031308
16. Kong P, Cui ZY, Huang XF, Zhang DD, Guo RJ, Han M. Inflammation and atherosclerosis: signaling pathways and therapeutic intervention. Signal Transduct Target Ther. 2022 Apr 22;7(1):131. doi: 10.1038/s41392-022-00955-7.
17. Björkegren JLM, Lusis AJ. Atherosclerosis: Recent developments. Cell. 2022 May 12;185(10):1630-1645. doi: 10.1016/j.cell.2022.04.004.
18. Bakić M, Patogenetski aspekti ateroskleroze, Acta Medica Medianae 2007;46(1):25-29.
19. Stary HC, Chandler AB, Dinsmore RE, Fuster V, Glagov S, Insull Jr W, et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1995 Sep 1;92(5):1355-74..
20. Meng H, Ruan J, Yan Z, Chen Y, Liu J, Li X, et al. New Progress in Early Diagnosis of Atherosclerosis. Int. J. Mol. Sci. 2022, 23, 8939. https://doi.org/10.3390/ijms23168939
21. Adam CA, Șalaru DL, Prisacariu C, Marcu DTM, Sascău RA, Stătescu C. Novel Biomarkers of Atherosclerotic Vascular Disease—Latest Insights in the Research Field. Int. J. Mol. Sci. 2022, 23, 4998. https://doi.org/10.3390/ijms23094998
22. Cao H, Zhu Y, Hu G, Zhang Q, Zheng L. Gut microbiome and metabolites, the future direction of diagnosis and treatment of atherosclerosis? Pharmacological Research. 2023 Jan;187:106586. DOI: 10.1016/j.phrs.2022.106586
23. Libby P. Inflammation in atherosclerosis—no longer a theory. Clinical chemistry. 2021 Jan;67(1):131-42.
