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This study aims to examine the influence of admission glycaemia and glycosylated haemoglobin (HbA1C) levels on the length of hospitalization and its outcome in insulin-independent diabetes mellitus (DM) patients suffering from ST-Segment Elevation Myocardial Infarction (STEMI)/Non-STEMI (NSTEMI). This cross-sectional study included 103 subjects with a history of insulin-independent DM, currently hospitalized due to acute myocardial infarction (AMI). Out of 103 subjects, 59 (57%) were men and 66 (64.1%) of them suffered from STEMI. Mean age of study population was 67±9 years. The following parameters were monitored: demographic, coronary, cardiovascular and DM risk factors history, as well as laboratory, clinical, echocardiography and angiography parameters. DM mean duration was 7 (1-30) months, and it influenced the length of hospitalization (r=0.232, p0.05). Mean length of hospitalization was 8 and 8.5 days in STEMI and NSTEMI patients respectively, with no difference between groups (log-rank ch2= 0.476, p>0.05). HbA1C values influenced the length of hospitalization (r=0.213, p0.05). Duration of DM and the level of HbA1C prolong the length of hospitalization, but do not influence the clinical outcome of AMI patients suffering from insulin-independent DM. Cilj prikazane studije je izučavanje uticaja glikemije i glikoziliranog hemoglobina (HbA1C) pri prijemu u bolnicu na dužinu trajanja hospitalizacije, kao i njen ishod kod kod obolelih od insulin-nezavisnog dijabetesa sa NSTEMI/STEMI. Materijal i metode: Ova studija je uključila 103 ispitanika, od kojih su 59 (57%) ispitanici muškog pola, a 66 (64.1%) ispitanika imalo STEMI. Prosečna životna dob ispitivane populacije je bila 67±9 godina. Praćeni su sledeći parametri: demografske karakteristike, anamneza o koronarnim, kardiovaskularnim i rizičnim faktorima za dijabetes, kao i laboratorijski, klinički, ehokardiografski parametri. Rezultati: Prosečno trajanje dijabetesa kod osoba uključenih u studiju je bilo 7 (1-30) meseci i imalo je uticaj na dužinu hospitalizacije (r=0.232, p0.05). Prosečno trajanje hospitalizacije je bilo 8 i 8.5 dana kod ispitanika sa STEMI i NSTEMI i nije se razlikovalo među grupama ispitanika (log-rank ch2= 0.476, p>0.05). Nivoi HbA1C su uticali na dužinu trajanja hospitalizacije (r=0.213, p0.05). Zaključak: Dužina trajanja DM i nivo HbA1C produžavaju dužinu hospitalizacije, ali ne utiču na klinički ishod ispitanika sa insulin-nezavisnim dijabetesom koji su doživeli AIM.

Insulin-zavisni dijabetes (IDDM, engl. Insulin-Dependant Diabetes Mellitus) se definiše kao stanje hronične hiperglikemije, odnosno povišne koncentracije glukoze u krvi uzrokovane poremećajem sekrecije hormona insulina. Hiperglikemija doprinosi disfunkciji endotela krvnih sudova, što dovodi do vaskularnih komplikacija i tkivne hipoksije. Uzimajući u obzir da poremećen balans kiseonika u plazmi ima važnu ulogu u patogenezi DM, primena terapije kiseonikom pod hiperbaričnim uslovima (HBK) je preporučena kako bi se usporio razvoj vaskularnih komplikacija. Terapija HBK ostvaruje antiaterogene, antioksidativne i kardioprotektivne efekte utičući na promenu nivoa i sastava masnih kiselina (MK), kao i prenos signala kroz membrane, narušen hiperglikemijom i hipoksijom. Pokazano je da HBK utiče na signalne molekule preko kojih insulin ostvaruje dejstvo, kao što su: supstrat receptora za insulin 1 (IRS-1, engl. Insulin Receptor Substrate), fosfatidilinozitol 3 kinaza (PI3K, engl. Phosphatidylinositide 3 Kinase), protein kinaza B (Akt, engl. Protein Kinase B), kinaze regulisane vanćelijskim signalima 1 i 2 (ERK1/2, engl. Extracellular Signal-Regulated Protein Kinases 1 and 2), nuklearni faktor kappa B (NFκB) i inducibilna azot-monoksid-sintaza (iNOS, engl. Inducible Nitric Oxide Synthase), i tako ostvaruje antiinflamatorne efekte kod pacijenata sa DM. U ovoj doktorskoj disertaciji učestvovalo je 28 pacijenata kojima je postavljena dijagnoza IDDM sa vaskularnim komplikacijama. Terapija HBK je podrazumevala izlaganje ispitanika 100% kiseoniku pod pritiskom do 2,4 apsolutnih atmosfera (ATA) u hiperbaričnoj komori u trajanju od jednog sata dnevno, tokom 10 tretmana. Pre početka i nakon tretmana HBK sakupljeni su uzorci krvi ispitanika, iz kojih su izolovani plazma, serum, i limfociti. Iz uzoraka krvi pacijenata mereni su nivo HbA1c, glikemija, koncentracija insulina, lipida, fosfolipida, slobodnih MK (SMK), C-reaktivnog proteina (CRP), azot-monoksida (NO, engl. Nitric Oxide), homocisteina (Hcy), kao i aktivnost arginaze. Primenom metode gasne hromatografije meren je udeo pojedinačnih MK u plazmi... Insulin-dependent diabetes mellitus (IDDM) is defined as a condition of a chronic hyperglycemia, i.e. elevated blood glucose level caused by impaired secretion of the hormone insulin. Hyperglycemia contributes to endothelial dysfunction, leading to vascular complications and tissue hypoxia. Given that impaired oxygen balance in plasma plays an important role in the pathogenesis of DM, administration of hyperbaric oxygen (HBO) therapy has been recommended to slow the development of vascular complications. HBO therapy exerts anti-atherogenic, antioxidant, and cardioprotective effects by altering the level and composition of plasma fatty acids (FA), thereby promoting signal transduction through the membrane, which is impaired by hyperglycemia and hypoxia. Also, the literature indicates that HBO affects molecules involved in the mechanism of insulin action, such as insulin receptor substrate (IRS-1), phosphatidylinositol 3 kinase (PI3K), protein kinase B (Akt), as well as deactivation of extracellular signal-regulated kinases 1 and 2 (ERK1/2), nuclear factor kappa B (NFκB), and inducible nitric oxide synthase (iNOS), thus exerts anti-inflammatory effects in patients with DM. This doctoral dissertation involved 28 patients with diagnosed IDDM and vascular complications. HBO treatment implies therapeutic inhalation of 100% oxygen under elevated pressure up to 2.4 absolute atmospheres in a hyperbaric chamber for one hour per day, during 10 treatments. Blood samples were collected from IDDM patients, and separated into plasma, serum and lymphocytes before starting therapy and after 10 th HBO treatment. Blood samples from IDDM patients were used for the measurement of HbA1c and glycemic levels, the concentration of insulin, lipids, phospholipid, free FA (FFA), C-reactive protein (CRP), nitric oxide (NO), homocysteine (Hcy), as well as for arginase activity. Gas chromatography method was used for measurement of the content of individual FA in plasma...

Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.

Metabolic syndrome (MetS) is a leading public health and clinical challenge worldwide. MetS represents a group of interrelated risk factors that predict cardiovascular diseases (CVD) and diabetes mellitus (DM). Its prevalence ranges between 10 and 84%, depending on the geographic region, urban or rural environment, individual demographic characteristics of the population studied (sex, age, racial and ethnic origin), as well as the criteria used to define MetS. Persons with MetS have higher mortality rate when compared with people without MetS, primarily caused by progressive atherosclerosis, accelerated by pro-inflammatory and pro-coagulation components of MetS. Considering the high prevalence of metabolic disorders (glucose metabolism disorder, hypertension, dyslipidaemia, obesity etc.), preventive healthcare should focus on changing lifestyle in order to reduce obesity and increase physical activity. This narrative review considers the available evidence from clinical and experimental studies dealing with MetS, and current treatment options for patients with insulin resistance and MetS.

U okviru ovog rada prikazan je slučaj bolesnika sa komplikovanim akutnim dislipidemijskim pankreatitisom u čijem je zbrinjavanju učestvovao tim, koji su činili endokrinolozi, gastroenterolozi i transfuziolozi. Dislipidemija, prevashodno tip IV dislipidemije, predstavlja čest uzrok nastanka akutnog pankreatitisa u populaciji mladih ljudi, posebno u slučajevima nezadovoljavajuće komplijanse (neredovno uzimanje preporučenih fibrata i nepridržavanje higijensko-dijetetskog režima). Tretman akutnog pankreatitisa se nezavisno od etiologije, zbog težine stanja, kompleksnosti lečenja i monitoringa bolesnika, sprovodi u Jedinicama intenzivnog lečenja. U slučajevima kada je dislipidemija uzrok akutnog pankreatitisa, često se u sklopu akutnog zbrinjavanja sprovodi i terapijska izmena plazme, kojom se brzo i značajno koriguju nivoi lipida, prevashodno triglicerida. Terapijska izmena plazme zahteva aktivnost transfuzioloških ekipa, koje su u manjim centrima, često nedostupne. This article presents a case of patient with acute and complicated dyslipidaemic pancreatitis, managed by team, consisted of the endocrinologists, gastroenterologists and transfusiologists. Dyslipidaemia, predominantly type IV, is a common cause of acute pancreatitis in young patients, especially in the cases of poor compliance (irregular taking of recommended fibrates and failure to comply with the dietary regime). The treatment of acute pancreatitis, regardless of the aetiology, is due to the severity of the condition, the complexity of the treatment, and the monitoring of patients, in the Intensive Care Units. In cases where dyslipidaemia is the cause of acute pancreatitis, in the context of acute care, a therapeutic plasma exchange is often performed. It rapidly and significantly corrects lipid levels, primarily triglycerides. Therapeutic plasma exchange requires the activity of transfusiology team, which are often unavailable in smaller hospitals.

Apoptosis may contribute to a significant proportion of neuron death following acute brain ischemia (ABI), but the underlying mechanisms are still not fully understood. Brain ischemia may lead to stroke, which is one of the main causes of long-term morbidity and mortality in both developed and developing countries. Therefore, stroke prevention and treatment is clinically important. There are two important separate areas of the brain during ABI: the ischemic core and the ischemic penumbra. The ischemic core of the brain experiences a sudden reduction of blood flow, just minutes after ischemic attack with irreversible injury and subsequent cell death. On the other hand, apoptosis within the ischemic penumbra may occur after several hours or days, while necrosis starts in the first hours after the onset of ABI in the ischemic core. ABI is characterized by key molecular events that initiate apoptosis in many cells, such as overproduction of free radicals, Ca2+ overload and excitotoxicity. These changes in cellular homeostasis may trigger either necrosis or apoptosis, which often depends on cell type, cell age, and location in the brain. Apoptosis results in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. This review focuses on recent findings based on animal and human studies regarding the apoptotic mechanisms of neuronal death following ABI and the development of potential neuroprotective agents that reduce morbidity. The effects of statins on stroke prevention and treatment as well as on apoptotic mediators are also considered.

Apoptoza je evolutivno očuvan mehanizam programirane ćelijske smrti, koji ima važnu ulogu u fiziološkim procesima, kao što su embrionalno razviće, hromonima regulisana ćelijska smrt, funkcionisanje imunog sistema i uklanjanje oštećenih ćelija. Dva osnovna puta indukcije apoptoze su unutrašnji i spoljašnji. Dok unutrašnji put apoptoze može pokrenuti unutarćeljska akumulacija Ca 2+ jona, koja je praćena permeabilizacijom membrane mitohondrija i oslobađanjem pro-apoptotskih proteina iz mitohondrija u citoplazmu, spoljašnji put uključuje aktivaciju membransih receptora za TNF-a (engl. Tumor Necrosis Factor-a), kao što su TNFR-1 (engl. Tumor Necrosis Factor receptor 1), Fas, i TRAIL-R (engl. TNF-related apoptosis-inducing ligand receptors). Pored toga, postoji i perforin-granzim put koji uključuje aktivaciju citotoksičnih T-limfocita. Sva tri puta rezultiraju fragmentacijom DNK, degradacijom citoskeleta i nuklearnih proteina, unakrsnim povezivanjem proteina, formiranjem apoptotskih tela, ekspresijom liganada za receptore na fagocitima i na kraju fagocitozom. U ovoj reviji su objedinjeni podaci iz nedavno objavljenih studija koje su fokusirane na proteine uključene u proces apoptoze i molekularne mehanizme apoptoze. Razumevanje mehanizama apoptoze može da pruži korisne informacije i nove pristupe u prevenciji i razvoju novih terapija za različite bolesti. Apoptosis is evolutionary conserved, programmed pattern of cell death with an essential role in various physiological processes, such as normal cell turnover and embryonic development, hormone-regulated cell demise, aging, immune system functioning and development and removal of defective and harmful cells. There are two general pathways for activation of apoptosis: the intrinsic and extrinsic pathways. While the intrinsic apoptotic pathway can be triggered by a cytotoxic accumulation of intracellular Ca 2+ , followed permeabilization of mitochondrial membrane and release of pro-apoptotic proteins into the cytosol from mitochondria, the extrinsic mechanisms of apoptosis include the participation of death receptors of tumor necrosis factor-a (TNF-a), receptor superfamily such as TNFR-1, Fas, and TNF-related apoptosis-inducing ligand receptors (TRAIL-R) located on the plasma membrane. There is also the perforin-granzyme pathway that involves T-cell mediated cytotoxicity. All three pathways converge on the same execution pathway, resulting in DNA fragmentation, degradation of cytoskeletal and nuclear proteins, cross-linking of proteins, formation of apoptotic bodies, expression of ligands for phagocytic cell receptors and finally uptake by phagocytic cells. In this review we summarize data from recent studies focusing on apoptotic proteins that have been identified and molecular mechanisms of apoptosis. Understanding apoptotic mechanism might provide useful information and a new approach to prevention and development of new therapies for variety of diseases.

An altered hepatic lipid metabolism involves multifactorial pathologies such as hepatic inflammation, insulin resistance and oxidative stress. Immunity has an essential role in the regulation of glucose and lipid metabolism in the liver. Inducible nitric oxide (NO) synthase (iNOS) has been proposed as an important factor that interplays between immunity and energy metabolism and also in the pathogenesis of obesity-linked insulin resistance. In the liver, locally produced NO plays a protective role during inflammation, and the balance of NO protective and cytotoxic effects is very important. This review is focused on understanding the molecular mechanisms of iNOS regulation in the state of altered hepatic lipid metabolism, which is critical for developing new strategies for treatment of hepatic disorders.

Atherosclerosis is a life-long illness that begins with risk factors, which in turn contribute to the development of subclinical disease, followed by the establishment of overt cardiovascular disease (CVD). Thrombotic-occlusive complications of atherosclerosis are among the most widespread and costly health problems. Oxidized low-density lipoprotein (OxLDL) plays an important role in atherogenesis by promoting an inflammatory environment and lipid deposition in the arterial wall. As cardiovascular events occur in individuals without common risk factors, there is a need for additional tools that may help in CVD risk assessment and management. The use of biomarkers has improved diagnostic, therapeutic and prognostic outcome in cardiovascular medicine. This review elaborates on the value of circulating OxLDL as a biomarker of CVD. Three enzyme-linked immunosorbent assays (4E6, DLH3 and E06) using murine monoclonal antibodies for determination of OxLDL blood levels have been developed. However, none of these assays are currently approved for routine clinical practice. We identified studies investigating OxLDL in CVD (measured by 4E6, DLH3 or E06 assay) by searching the PubMed database. Circulating OxLDL was found to be associated with all stages of atherosclerosis, from early atherogenesis to hypertension, coronary and peripheral arterial disease, acute coronary syndromes and ischemic cerebral infarction. The results of studies investigating the usefulness of OxLDL for CVD prediction were also summarized. Furthermore, OxLDL was found to be associated with pathologic conditions linked to CVD, including diabetes mellitus, obesity and metabolic syndrome (MetS). In addition, we have addressed the mechanisms by which OxLDL promotes atherogenesis, and the effects of antiatherogenic treatments on circulating OxLDL. Finally, we highlight the evidence suggesting that lipoprotein (a) [ Lp(a)] is the preferential carrier of oxidized phospholipids (OxPL) in human plasma. A strong association between OxPLapoB level (representing the content of OxPL on apolipoprotein B-100 particles, measured by E06 assay) and Lp(a) has been determined.

The assessment of cardiovascular risk and treatment of cardiovascular diseases are major public health issues worldwide. Inflammation is now recognized as a key regulatory process that links multiple risk factors for atherosclerosis. The substantial number of patients having cardiovascular events lack commonly established risk factors. The utility of high-sensitivity C-reactive protein (hsCRP), a circulating biomarker related to inflammation, may provide additional information in risk prediction. This review will consider the impact of hsCRP level on initiation of statin therapy.

Estrogens have been recognized, in the last 3 decades, as important hormones in direct and indirect modulation of vascular health. In addition to their direct benefit on cardiovascular health, the presence of esterified estrogen in the lipid core of high-density lipoprotein (HDL) particles indirectly contributes to atheroprotection by significantly improving HDL quality and functionality. Estrogens modulate their physiological activity via genomic and nongenomic mechanisms. Genomic mechanisms are thought to be mediated directly by interaction of the hormone receptor complex with the hormone response elements that regulate gene expression. Nongenomic mechanisms are thought to occur via interaction of the estrogen with membrane-bound receptors, which rapidly activate intracellular signaling without binding of the hormone receptor complex to its hormone response elements. Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms. In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS. Nitric oxide primarily influences blood vessel relaxation, the heart rate, and myocyte contractility. The abnormalities in expression and/or functions of eNOS lead to the development of cardiovascular diseases, both in animals and in humans. Although considerable research efforts have been dedicated to understanding the mechanisms of action of estradiol in regulating cardiac eNOS, more research is needed to fully understand the details of such mechanisms. This review focuses on recent findings from animal and human studies on the regulation of eNOS and HDL quality by estradiol in cardiovascular pathology.

The pathogenesis of acute brain ischemia (ABI) is highly complex and involves multiple mechanisms including free radical generation. Imbalance between the cellular production of free radicals and the ability of cells to defend against them is referred to as oxidative stress. Oxidative stress is one of the mechanisms contributing to neuronal damage, potentially induced through the ABI. Through interactions with a large number of molecules, reactive oxygen species may irreversibly destroy or alter the function of the cellular lipids, proteins, and nucleic acids and initiate cell signaling pathways after cerebral ischemia. Future investigations should focus on the understanding of oxidative stress mechanisms and neuro-protection in order to discover new treatment targets.

Estrogens are secreted primarily by the ovaries and placenta, by the testes in men and also produced by peripheral steroidogenic conversion. The 3 major naturally occurring estrogens are: 17 beta-estradiol (E-2), estrone and estriol, of which E-2 is the predominant and most active. The actions of E-2 are mediated by at least 3 different receptors - the classical ERs (ER alpha and ER beta) and G-protein coupled receptor 30 (GPR30). E-2 signaling in cardiomyocytes involves ER alpha- and ER beta-independent pathways, and treatment with the E-2 receptor antagonists (Selective Estrogen Receptor Modulators- SERMs), which are agonists of GPR30, inhibits cardiac cell growth. Effects of E-2 in preventing endothelial dysfunction, a prerequisite of atherosclerosis, are well recognized. Atherosclerosis involves interaction between the cells of the arterial wall endothelial cells (EC) and vascular smooth muscle cell (VSMC), as well as migration of macrophages into wall tunica media. It is predominantly developed at sites with abnormally high shear stress, such as bifurcations or branching of arteries, initiated by an injury to the endothelium and exposure to atherogenic lipids and toxins, such as those contained in tobacco smoke or infectious agents. Animal studies have shown effects of E-2 in preventing atherosclerosis, inflammation and endothelial or vascular dysfunction. Gender differences along this pathogenic pathway have been also described. We review the data from the available animal and human studies, which focus on anti-atherogenic effects of E-2. These studies represent evidence, albeit indirect, for an inhibitory effect of E-2 on the progression of coronary artery atherosclerosis.

Biomarkeri predstavljaju indikatore normalnih bioloških procesa, patogenih procesa ili farmakoloških odgovora na terapijske intervencije. Interleukin-6 (IL6, engl. Interleukin-6) je biomarker, čija sinteza može biti aktivirana različitim stimulusima, kao što su: interferon-g (IFN-g, engl. Interferon-g), faktor tumorske nekroze (TNF, engl. Tumor Necrosis Factor) i/ili interleukin-1 (IL-1, engl. Interleukin-1). IL-6 svoje efekte ostvaruje preko IL-6 receptora (IL-6R, engl. IL-6 Receptor). Pokazano je da kod transgenih miševa, kod kojih je indukovana ekspresija IL-6 i IL-6R, dolazi do hipertrofije miokarda. U mehanizmu hipertrofije miokarda bitnu ulogu ima i novootkriveni kardiotrofin1 (CT-1, engl. Cardiotrophin-1) koji je jedan od članova IL-6 familije. Aktivnost IL-6 vezuje se za razvoj aneurizme abdominalne aorte (AAA, engl. Abdominal Aortic Aneurysm), zapravo, pokazano je da su aneurizme mesta odakle cirkuliše IL-6, a takođe se smatra da je koncentracija IL-6 u pozitivnoj korelaciji sa dijametrim AAA. C-reaktivni protein (CRP, engl. CReactive Protein) je jedan od mnogobrojnih biomarkera kardiovaskularnih bolesti. Uloga CRP-a je u nastanku i progresiji kardiovaskularnih bolesti. Lokalna produkcija CRP-a od strane glatkih mišićnih i endotelnih ćelija krvnog suda, u velikoj meri utiče na razvoj procesa ateroskleroze. Važnu ulogu u nastanku ateroskleroze, osim CRP-a, ima i oksidovani lipoprotein male gustine (ox-LDL, engl. Oxidized Low Density Lipoprotein). Oksidaciju LDL-a vrše različiti enzimi. Ox-LDL nakon što prođe u intimu krvnog suda indukuje sakupljanje monocita, tj. monociti se prevode u makrofage koji vezuju ox-LDL. Kada se makrofagi napune ox-LDL-om, dolazi do pokretanja signala ćelijske smrti i stvaraju se forme penušavih ćelija koje čine početni deo aterosklerotičnog plaka. Nova saznanja o mehamizmu delovanja kao i uloge biomerkera u nastanku kardiovaskularnih bolesti, svakako će pružiti jednu od mogućnosti prevencije nastanka ovih poremećaja, a takođe i adekvatnu terapiju u lecenju kardiovaskularnih oboljenja, što i jeste jedan od glavnih ciljeva intezivnih istraživanja u oblasti biomarkera. U ovom preglednom članku, opisana su tri biomarkera kardiovaskularnih bolesti: IL-6, CRP i LDL. Biomarkers are indicators of normal biological processes, pathogenic processes or pharmacologic responses to therapeutic interventions. Interleukin-6 (IL - 6) is a biomarker whose synthesis could be activated by various stimuli, such as interferon-g (IFN - g), tumor necrosis factor (TNF) and/or interleukin - 1 (IL - 1). IL - 6 achieves its effects through the IL-6 receptor (IL - 6R). It has been shown that transgenic mice, which have induced expression of IL - 6 and IL - 6R develop myocardial hypertrophy. In myocardial hypertrophy, an important role is played by a newly discovered cardiotrophin-1, a member of the IL - 6 family. The activity of IL - 6 is associated with the development of abdominal aortic aneurysm (AAA); in fact, it has been shown that the concentration of IL - 6 positively correlates with AAA diameters. C-reactive protein (CRP) is one of the biomarkers of cardiovascular diseases. Local production of CRP by the smooth muscular and endothelial cells of the vessel leads to the development of atherosclerosis to a large extent. Oxidized low-density lipoprotein (ox - LDL) also has an important role in the development of atherosclerosis. After penetrating the intima of the vessel, ox - LDL induces monocyte collection, i.e. monocytes are translated into macrophages that bind ox - LDL. Having filled the macrophages with ox - LDL, the signals of cell death are activated, which leads to the creation of foamy cells that make up the initial part of the atherosclerotic plaque. New knowledge about the mechanism of action and the role of biomarkers in the development of cardiovascular diseases will certainly provide an opportunity to prevent the onset of these disorders, as well as an adequate therapy in the treatment of cardiovascular diseases, which is one of the main goals of intensive research in the field of biomarkers.