Role of cytokines in the pathogenesis of chronic coronary syndrome

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Муминова, С., Нигмонов, Б., Расулев, Ё., & Юлдашова, Е. (2024). Role of cytokines in the pathogenesis of chronic coronary syndrome. in Library, 1(1), 517–521. извлечено от https://inlibrary.uz/index.php/archive/article/view/32706
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Аннотация

The present-day perceptions of inflammation role in ischemic heart disease are reviewed. Recent
investigations resulted in the cmciging of a new idea of atherosclerosis - the majority of the researchers consider atherosclerosis to be a chronic inflammatory process of low -grade intensity accompanied by the cytokines dischaigc by the blood and endothelial cells which possess the property to activate and inhibit inflammation. Athcrothrombosis is the final stage of this process and the main cause of myocardial infarction. The possible ways of intervention into this process in the treatment of cardiovascular diseases arc discussed.

Похожие статьи


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517

Muminova S.U. Nigmonov B.B. Rasulev Y.E. Yuldashova Y.X.

ROLE OF CYTOKINES IN THE PATHOGENESIS OF CHRONIC CORONARY SYN-

DROME

Tashkent pediatric medical institute

Introduction

The present-day perceptions of inflammation role in

ischemic

heart

disease

are

reviewed.

Recent

investigations resulted in the cmciging of a new idea of
atherosclerosis - the majority of the researchers consider
atherosclerosis to be a chronic inflammatory process of
low -grade intensity accompanied by the cytokines
dischaigc by the blood and endothelial cells which
possess the property to activate and inhibit
inflammation. Athcrothrombosis is the final stage of this
process and the main cause of myocardial infarction.
The possible ways of intervention into this process in
the treatment of cardiovascular diseases arc discussed.

Cardiovascular disease (CVD) continues to be the

leading cause of death in all the world. This mainly
applies

to

diseases

associated

with

common

pathogenesis - atherosclerosis, the most important factor
in the development of coronarv heart disease (IHD).

The point of view is becoming generally accepted.

according to w hich the most real factor in the initiation
and progression of IHD is inflammation, and
destabilization atherosclerotic plaque is detennined by
the high activity of the current chronic inflammatory
process. Research in molecular biology allow ed to
obtain convincing evidence of the participation of
cytokines in the process of damage to atherosclerotic
plaque in the coronary vessel as a result of its
inflammation and rupture. This is the main mechanism
leading to the development of acute coronary events -
unstable angina pectoris (NS), myocardial infarction
(MI) and sudden death [5,6,28, 33,39].

Hie inflammatory theory of atherogenesis is

confirmed detection in the blood of CVD patients, first
of all. an increased concentration of markers of the
inflammatory response, such as cytonins IL-1 b, IL6.1L-
I0.TNF- a, adhesion molecules, etc. 11]. IL-6 is a
multifunctional

cytokine

and

stimulates

the

proliferation of T-lymphocytes, macrophages, endo-
thelial cells 1111. With the help of IL-6, endothelial
cells, monocytes arc activated and procoagulative
reactions occur [8,10]. Cytokines have a strong effect on
the production of each other. In this network of mutual
influences, almost all effects arc stimulating. and only
IL-6 suppresses the production of IL-1 and TNF- a. Tins
the peculiarity of IL-6 dctcnnincs its dual role in
development of inflammation: being a typical pro-
inflammatory cytokine in its effects, it also has an anti-
inflammatory cflcct. Biological the meaning of this

phenomenon boils dow n to the fact that IL-6, as it were
completes the formation of the inflammatory process.

Tire main functions of IL-6 also include stimulation

synthesis of proteins of the acute phase of
inflammation, antibodies, activation of endothelial
cells and hyperthennia |38|. Relatively recently it was
found that high FC of angina pectoris arc accompanied
by cytokine hyperexcretion. This indicates the
presence already at the stage of stable angina pectoris
persistent inflammation, which, in its turn, increases
the risk of thrombotic complications and ACS [2].

IL-1 b is a secretory cytokine that acts both locally

and at the systemic level |4|. Experiments have shown
that IL-lb has no less than 50 different biological
functions, and almost all organs and tissues arc targets.
One relatively small molecule stimulates development a
whole complex of protective reactions of the div,
armed at limiting the spread of infection, restoring tire
integrity of damaged tissues. An integral part of the
biological action of IL-lb is a stimulating effect on the
metabolism of connective tissue. Tire mediator
stimulates the proliferation of fibroblasts and increases
their production prostaglandins. growth factors and a
number of cytokines 19].

One of the pro-inflammatory cytokines directly

involved in inflammation in atherosclerosis is tumor
necrosis factor - a (TNF- a). TNF-is predominantly
produced by monocytes / macrophages, endothelial
cells and mast cells. TNF-aflects the endothelium,
enhances the expression of adhesion molecules on it.
activates macrophages, neutrophils, causes the synthesis
of acute phases of inflammation. Disruption of TNF-
mctabolism undoubtedly plays a role in the
development of CVD. |38, 46]. It was found that
postischemic reperfusion the myocardium is ac-
companied by an increase in the level of cytokine.
According to some reports, tire level of TNF-in serum
increases both in patients w ith unstable and in patients
with stable angina pectoris II1-IV functional class 17,
211. TNF production tn the acute post-infarction period
is triggered mainly by ischemia.

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518

In the early postinfarction phase, a certain degree of
mediator production is physiological, because during
this period cytokines play a protective role in decreasing
cell apoptosis [25, 35]. In experimental models, the
actual immediate inotropic effect of TNF-was obtained,
which lasts until complete elimination of the cytokine.
However, this cytokine not only has a negative inotropic
effect, it summarizes cellular and biochemical disorders
found in cardiac damage muscles. TNF-causes a
hypertrophic response the grow th of cardiomyocytes,
which is an adaptation to hemodynamic disturbances
1221.

Cytokines play a major role in the pathogenesis of

atherosclerosis. Some of them may show anti-ath-
erogenic and anti-inflammatory effects by inhibiting
TNF and IL-6. This cytokine is IL-10 [23]. Data on the
presence and action of IL-10 in the ischemic
myocardium were obtained in studies experimental
models of myocardial infarction [24, 32,44]. In the
course of experiments on dogs, direct evidence w as
obtained that IL-10 is formed in the myocardium during
ischemia and reperfusion [231.

The authors especially emphasize the significant

increase in the expression of IL-10 during the
resumption of myocardial circulation and suggest that
this is probably a consequence of the increased access
of lymphocytes to the ischemic zone caused by
reperfusion. In tire recovering myocardium, the main
sources of IL-10 synthesis arc T-lymphocytes [ 16]. The
produced cytokine plays a special role in scar formation
in the damaged area. In the absence of experimental
animal gene responsible for IL-10 production,
inflammatory response after MI was more pronounced
compared to ordinary animals. In this group of
experimental animals, an increase in the size of the MI
zone, an increase in the level of TNF-and the expression
of MCP-1 was determined 1441. So Thus, endogenous
IL-10 plays a protective role in the time of myocardial
ischemia / reperfusion as a result of a decrease in the
acute inflammatory process. IL-10 is a potent monocyte
dcactivator and suppressor various pro-inflammatory
cytokines.

It is proved that IL-10 reduces the severity of the

inflammatory response and leads to improved LV
function and remodeling processes [29]. An inverse
relationship was found between the level of













IL-10 and the severity of exertional angina.
Like cells in other tissues, tissues of the car-

diovascular system arc not only producers, but also
targets of another inflammatory mediator - TGF-b
(transforming growth factor b It was found that TGF-b
promotes an increase in the time of tolerance of hypoxia
by cardiomyocytes |42.431 and an increase in
proliferation of myofibroblasts [20]. Introducing TGF-b
in animals before the induction of ischemia or

immediately after it reduced the rate of pathological
changes in the myocardium 130]. The authors believe
that this cytoprotective effect of TGF-is due to
inhibition of the release of TNF-into the circulatory
system. Data on the regulatory effect of TGF-on
homeostasis and functional activity of blood vessel cells
indicates its ability to influence the formation of new
capillaries. Thus, TGF-b is involved in the regulation of
a large number of vital functions of cells of the

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519

cardiovascular system through cell proliferation and
migration, and also keeping them alive. Special
molecules, integrins, play an important role in
intercellular interactions and triggering cytokine
cascades |31. In atherosclerosis. intercellular adhesion
molecules (ICAMs) should be isolated. The role of
molecules of the ICAM group is most significant in the
migration of leukocytes to the inflammation focus.
1CAM-1 is expressed under the influence of activation
by cytokines such as IL-lb TNF-a a interferons. Re-
vealed increase concentration of soluble ICAM-1 in
blood plasma in patients with ACS, as well as after
episodes of anginal pain in patients wdth unstable
angina pectoris or myocardial infarction (MI) without Q
wave [31]. The high level of soluble ICAM-1 persisted
for 6 month An increase in the level of MCP-1
(monocytic chemotactic protein-1) in blood plasma is
observed in patients with coronary artery disease, and
the highest values arc determined during ACS 112, 19].
Increased levels of circulating MCP-I have a positive
correlation with most risk factors for CVD [18, 39].
During studies of patients who underwent ACS. it was
found that an increase in the level of MCP-1 more than
238 pg / ml is a predictor of mortality in the same way
like CRP and BNP. It was found that MRS-1 through
activation macrophages can cause destabilization of
atherosclerotic plaque, and thereby cause an episode of
my ocardial ischemia [ 17]. In an experiment on rats
with by modeling MI, the administration of antibodies
to MCP-1 leads to a decrease in the size of die infarction
zone, which was explained by a decrease in the
expression of adhesion molecules and infiltration by
macrophages, as well as to a decrease in ventricular
dilatation and preservation of contractile function [26].
The classic option for the treatment of coronary artery
disease is the restoration of coronary blood flow.
Opening of special molecules capable of stimulating
angiogenesis in the myocardium contributed to the
growth of interest in the implementation of flicse know
ledge into practice. The increase in angiogenesis is
explained by the activation of growth factors, mainly of
die family

VEGF (vascular endodielial growth factor).

However, the role VEGF in atherosclerosis and
coronary artery disease is dual: there are clinical
experimental data in favor of the participation of VEGF
in stimulating the growth of atherosclerotic plaques
[39]. The literature indicates diat hopes for the
therapeutic effect of angiogenic factors in ischemia my
ocardium as a whole was not confirmed [40].
Established that VEGF. acting in combination with
other factors growth and cell receptors, stimulates the

proliferation of mesenchymal cells [13], this can
contribute to the development of fibrosis and
atherosclerosis. Besides Moreover, VEGF can enhance
vascularization of atherosclerotic plaques, contributing
to their instability 115]. The benefit of local
angiogenesis in the ischemic zone is questionable, since
ischemia is usually caused by obstruction of die vessels
located in die epicardium, and the narrow ing is located
proximal to the focus ischemia. Therefore, weakening
of ischemia can be facilitated by functioning collaterals,
but not by enhancement of microcirculation in the
ischemic zone [34, 36]. With the establishment of the
role of inflammatory processes in the development of
atherosclerosis, determination of plasma levels of
inflammation has become an important tool for
predicting cardiovascular risks. Recent data assign a
special role to die pro-inflammatory cytokine IL-
18.

It is a pleiotropic proinflammatory cytokine that

plays a leading role in triggering die inflammatory
cascade [24]. Recently, in experimental studies, it was
found that the expression of IL-18 is closely associated
w ith the progression and instability of atherosclerotic
plaque. According to the AthcroGcnc Study, the
concentration of circulating IL-18 is a harbinger of
future acute conditions in patients w ith stable and
unstable angina pectoris 1141. The main function of the
IL-18 is to launch production of interferon- a and
triggering the Till response. IL-18 stimulates the
expression of IL-6, ICAM-1. mononuclear phagocytes
and a number of other chemokines, has a strong
regulatory activity on NK cells. IL-18 can cause an
increase in the production of IL-1 b TNF- a IL-6, etc.)
with the onset of myocardial infarction was established,
of course, and the assumption that a decrease in the
severity of inflammation may be accompanied by a
decrease in the likelihood the development of
complications of myocardial infarction. So far only
evidence is accumulating that various interventions can
low er levels of inflammatory markers. Considering the
current state of die issue of the inflammatory component
of a heart attack myocardium, it is advisable to assess
die dy namics of the cytokine profile during treatment,
which makes it necessary to study possible ways of
influencing of that.


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Библиографические ссылки

Братусь, В.В. Атеросклероз, ишемическая болезнь сердца, острый коронарный синдром. В.В. Братусь, В.А.Шумаков, ТВ. Талаева. Киев: Четверта хвиля, 2004:576.

Закирова, Н.Э. Иммуновоспалительные реакции при ишемической болезни сердца. Н.Э. Закирова, Н.Х. Хафизов, И М. Карамова. Рациональная фармакотер. в кард. 2007;2:16-19

Залесский В.Н. Апоптоз при ишемии и реперфузии миокарда. В.Н.Залесский, Т.Н. Гавриленко А.А. Фильченков. ЛУкарьска справка. 2002;1:21-24.

Кашкин, К.П. Цитокины иммунной системы: основные свойства и иммунобиологическая активность. Клин. лаб. диагностика. 1998;11:21-32.

Королева, ОС. Биомаркеры в кардиологии регистрация внутрисосудистого воспаления. ОС. Королева, Д.А. Затейщиков. Фарматека. 2007;8-9:30-36.

Литвин, Е.И. Динамика экспрессии цитокинов у больных с острым коронарным синдромом. Укр. кардиол. журнал. 2002;1:21-24.

Лутай, М.И. Атеросклероз: современный взгляд на патогенез. М.И.Лутай. Украинский медицинский журнал. 2004; 1: 22-34.

Маянский, А Н. Современная эволюция идей И И. Мечникова о внутрисосудистом воспалении. А Н.Маянский. Иммунология. 1995;4:8-14.

Симбирцев А С. Новые подходы к клиническому применению Беталейкина реком- бинатного интерлейкина-1ЬТалаева, ТВ. Механизмы инициации острого коронарного синдрома: роль модифицированных липопротеинов как аутоантигенного фактора. ТВ.Талаева, Е.Н. Амосова, В.В. Братусь. Украинский кардиол журнал. 2006;9:18-24.

Титов, В.Н. Общность атеросклероза и воспаления: специфичность атеросклероза как воспалительного процесса (гипотеза). Биохимия. 2000;4:3-10.

Aukrust, Р. Interaction between chemokines and oxidative stress: possible pathogenic role in acute coronary syndromes. P.Aukrust, R.K.Berge, T. Ueland. J. Am.Coll. Cardiol. 2001;37:485-491.

Ball, S.G. Vascular endothelial growth factor can signalthrough platelet-derived growth factor receptors. S.G. Ball, C.A. Shuttleworth, C M. Kielty. J. Cell. Biol. 2007;177(3):489-500.

Blankenberg, S. Interleukin-18 is a strong predictor of cardiovascular death in stable and unstable angina. S. Blankenberg, L. Tiret, C. Bickel. Circulation. 2002;106:24-30.

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