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Badacz, R.;  Przewłocki, T.;  Legutko, J.;  Żmudka, K.;  Kabłak-Ziembicka, A. microRNAs Associated with Carotid Plaque Development and Vulnerability. Encyclopedia. Available online: https://encyclopedia.pub/entry/38899 (accessed on 22 December 2025).
Badacz R,  Przewłocki T,  Legutko J,  Żmudka K,  Kabłak-Ziembicka A. microRNAs Associated with Carotid Plaque Development and Vulnerability. Encyclopedia. Available at: https://encyclopedia.pub/entry/38899. Accessed December 22, 2025.
Badacz, Rafał, Tadeusz Przewłocki, Jacek Legutko, Krzysztof Żmudka, Anna Kabłak-Ziembicka. "microRNAs Associated with Carotid Plaque Development and Vulnerability" Encyclopedia, https://encyclopedia.pub/entry/38899 (accessed December 22, 2025).
Badacz, R.,  Przewłocki, T.,  Legutko, J.,  Żmudka, K., & Kabłak-Ziembicka, A. (2022, December 16). microRNAs Associated with Carotid Plaque Development and Vulnerability. In Encyclopedia. https://encyclopedia.pub/entry/38899
Badacz, Rafał, et al. "microRNAs Associated with Carotid Plaque Development and Vulnerability." Encyclopedia. Web. 16 December, 2022.
microRNAs Associated with Carotid Plaque Development and Vulnerability
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This entry is adapted from the peer-reviewed paper 10.3390/ijms232415645

Ischemic stroke (IS) related to atherosclerosis of large arteries is one of the leading causes of mortality and disability in developed countries. Atherosclerotic internal carotid artery stenosis (ICAS) contributes to 20% of all cerebral ischemia cases. Atherosclerosis prevention and treatment measures aim at controlling the atherosclerosis risk factors, or at the interventional (surgical or endovascular) management of mature occlusive lesions. Studies emphasize that microRNA (miRNA) are the emerging particles that could potentially play a pivotal role in this approach.

atherosclerosis atherosclerotic risk factors carotid artery stenosis carotid plaque cerebrovascular ischemia endothelial cells microRNAs plaque vulnerability platelets vascular smooth muscle cells

1. Introduction

Ischemic stroke (IS) is one of the leading causes of mortality and disability in developed countries [1]. Atherosclerotic internal carotid artery stenosis (ICAS) accounts for about 20% cases of cerebral ischemia [2]. The present diagnostic tools for carotid artery assessment are based on imaging studies, including carotid Doppler ultrasonography, computed tomography, magnetic resonance, or conventional invasive angiography with a use of intravascular ultrasound (IVUS), and optical coherence tomography (OCT) [3][4][5]. They display the degree of ICAS, as well as carotid plaque morphology [6].
The current guidelines position carotid endarterectomy (CEA) and carotid artery stenting (CS) as the established treatment methods for ICAS [7]. In addition to invasive treatment, the optimal medical approach, including cardiovascular risk factor-control, as well as pharmacotherapy (i.e., antiplatelet and antidiabetic agents, lipid and blood pressure lowering medication), should be introduced in order to reduce IS risk [8][9]. The optimal timing for the intervention on carotid artery is controversial [10][11]. According to guidelines, CEA or CS is recommended in recently symptomatic ICAS with stenosis severity above 50% lumen reduction [10][11], whereas the intervention on asymptomatic ICAS is recommended in high-grade stenosis, or in carotid plaques exceeding 60% lumen reduction when features of high-risk plaque for cerebral ischemia are present [10]. As IS can result from a fragmented plaque debris release with a subsequent embolization of cerebral arteries, plaque rupture followed by local carotid artery thrombosis, or hypoperfusion of cerebral structures, the mechanism of cerebral ischemia is complex [12][13][14][15]. Thus, as evidenced, plaque morphology and structure, in addition to the degree of carotid artery stenosis, play the pivotal role in the IS risk assessment and decision on the intervention [16].
The serious drawback of the aforementioned imaging tools is that they do not allow for the assessment of early stages of atherosclerosis, i.e., those that precede intima-media complex thickening and early fatty lesions incidences [17]. Unfortunately, current guidelines miss laboratory biomarkers which could predict the incidence of IS and thus target the high-risk group of patients with preemptive treatment, whereas early intervention upon the initiation of atherosclerosis seems very attractive [18]. Data show the important roles of pro-atherothrombotic and pro-inflammatory biomarkers, including cytokines (IL-1β, IL-6, TNFα), platelets, and macrophages activity [19][20][21].
Recent studies emphasize that microRNA (miRNA) are the emerging particles that could potentially play a pivotal role in this approach [22]. miRNAs are small, non-coding RNA nucleotides, having a length that is typically between 18 and 27 nucleotides that regulate post-transcriptional gene expression, by binding to the 3′- (more often), or to 5′-untranslated regions of mRNA, or exons [23]. The role of the miRNA has already been confirmed in the broad range of both physiological and pathological processes [24]. They are responsible for target gene expression regulation after the transcription process, either by inhibiting the translation or mRNA degradation [25]. The diagnostic and prognostic role of circulating miRNAs in ICAS leading to IS has been studied, however the conclusions remain inconsistent.

2. From Fatty Streaks and Foam Cells to Mature Plaque

Plaque formation initiates from stages that are not detectable by imaging tools [26]. First stages include endothelium dysfunction, accompanied by inflammation and modified low-density lipoprotein (LDL) retention in the intimal layer of the intima-media complex [27]. In the endothelium equilibrium, a great number of miRNAs are involved, including protective ones [28]. Their protective effect is achieved through many signaling pathways, however their major role is to prevent unfavorable lipid metabolism and reduce inflammation [28]. One of these miRNAs, miR-126, protects endothelial cells (ECs) through the suppression of NOTCH-1 inhibitor and activation of the vascular endothelial growth factor (VEGF) signaling (Table 1) [29][30]. At the beginning, miR-155 induces the downregulation of mitogen-activated protein 3 kinase 10 (MAP3K10), endothelin-1 (ET-1), and angiotensin II (ANG II) type I receptor [31][32]. The downregulation of ET-1 is important in many cardiovascular settings, as elevated levels of ET-1 are independently associated with increased cardiovascular mortality [33][34]. miR-146a and miR-125a decrease the lipid uptake in macrophages [35][36]. miR-146a also inhibits endothelial activation by increasing nitric oxide synthase (eNOS) expression [35]. miR-125 modulates extracellular vascular endothelial growth factor (VEGF) by manipulating macrophage soluble VEGF receptor-1 (sVEGFR1) production. This mechanism has a therapeutic potential in many diseases [36]. miR-206 and miR-223 regulate cholesterol synthesis through the reverse cholesterol transport from macrophages to the liver for excretion, attenuates pro-inflammatory cytokine production, and has a role in platelet activation [37][38][39][40][41].
Table 1. Critical miRNAs participating in atherosclerotic carotid artery lesions development: from fatty streaks to mature plaque: a therapeutic approach.
Critical Stages in Atherosclerosis miRNA Mechanism Effect of miRNA Action Therapeutic Approach (HUVEC or Animal Studies) Ref.
Initiation and early atherosclerosis          
‘Brakes’ of atherosclerosis          
Promotes ECs proliferation and repair, protects ECs miR-126-5p suppression of the Notch1 inhibitor Dlk1 At non-predilection sites, high miR-126-5p levels in ECs confer a proliferative reserve that compensates for the antiproliferative effects of hyperlipidemia T, injection of miR-126-5p rescued ECs proliferation at predilection sites and limited atherosclerosis [29]
Decreases atherosclerosis progression miR-155 downregulation of MAP3K10
downregulation of ET-1 and ANG II type I receptor		 Down-modulates inflammatory cytokine production T, the miR-155 mimic decreased IL-6, MMP-9 and TNF-α secretions of oxLDL-induced macrophages [31][32]
Decreases lipid uptake in macrophages, inhibits endothelial activation miR-146a regulates TLR4, increases eNOS expression Inhibits ox-LDL and inflammatory response (decreases IL-6, -8, MMP-9) Overexpression may be useful [35]
Macrophage polarization MiR-125a downregulation of sVEGFR1 Decreases lipid uptake in macrophages, modulates extracellular VEGF by manipulating sVEGFR1 T, miR-125a-5p inhibition reduces VEGF through the increased sVEGFR1 [36]
Increase reverse cholesterol transport from macrophages to the liver for excretion miR-206
miR-223		 promote efflux
promote efflux		 crucial for the prevention of lipid accumulation and atherosclerosis T, these miRs can be efficiently delivered to macrophages via chitosan nanoparticles [39][40]
Prevents ECs senescence miR-let-7g Stimulates anti-aging gene SIRT1, and IGF 1,
inhibits expression of LOX-1		 exert anti-aging effects on ECs T, antagonizing endogenous
let-7 has induced cell
proliferation		 [42]
Prevents ECs senescence miR-143 targets a network of transcription factors, including KLF4, myocardin, and Elk-1 promotes differentiation and repress proliferation of VSMCs microvesicles containing miR-143 injected into mice could reduce the formation of atherosclerotic plaques [43][44]
Suppresses atherosclerotic plaque formation miR-520 targets RelA/p65 regulates VSMCs decreasing migration and proliferation miR-520c-3p agomir decreased atherosclerotic plaque size [45]
High expression is needed to maintain a contractile phenotype of VSMCs miR-22 multiple target genes induce the phenotypic switch from synthetic to contractile T, the stent with the miR-22 coating showed significant capability to inhibit in-stent restenosis [46]
Promotors of atherosclerosis          
Increases endothelial inflammation miR-92a regulation of KLF2 markedly enhanced by hypercholesterolemia T, inhibition of miR-92a reduces endothelial inflammation and atheroma plaque size [47]
Vascular senescence, vascular calcifications
Altered lipid metabolism
Increases inflammatory
cytokines secretion of macrophages M1		 miR-34a inhibition of SIRT1 and AXL receptor tyrosine kinase
targets cholesterol transporters: ABCA1 and ABCG1
through the nuclear hormone LXRα		 aggravates and accelerates vascular senescence
increase the binding capacity
of oxLDL to macrophages
stimulate pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12, IL-23), and chemokines (CCL5, CCL8, CXCL2, CXCL4)		 T, inhibition with antago-miR-34a [48][49]
Promotes cholesterol accumulation in macrophages, decreases reverse cholesterol transport miR-33a Targets hepatic ABCA1 inhibit efflux, increases macrophages ox-LDL uptake, foam cells accumulation T, inhibition of miR-33a facilitates atherosclerosis regression [50][51]
Promotes atherosclerosis miR-155 repressing Bcl6 in macrophages, suppress eNOS increases pro-inflammatory NF-κB signaling, down-regulates the expression of eNOS and production of NO T, inhibition of miR-155 increased eNOS expression and NO production [32][52]
Increases apoptosis in ECs miR-17-5p repression of ABCA1 expression through directly binding to its 3′-UTR rate of apoptosis in ECs T, inhibition of miR-17 suppresses apoptosis, hence decrease infarct size area, and improves microcirculation of the heart tissue, decreasing heart failure symptoms [53][54]
Promotion of monocyte adhesion, proinflammatory
Lipid metabolism		 miR-21 targets PPAR α
targets TLR4 and NF-κB		 enhances the expression of VCAM-1 and MCP-1 and the adhesion of monocytes to ECs
LPS-induced lipid accumulation and inflammatory response
in macrophages		 Overexpression of miR-21 up-regulated ATP-1 activation, which was attenuated by exogenous expression of PPARα
overexpression of miR-21 significantly decreased the secretion of IL-6 and increased IL-10 levels		 [55][56]
Induces ECs apoptosis, development of atherosclerosis miR-142-3p up-regulation of Rictor and the Akt/eNOS atherosclerosis-associated
ECs apoptosis		 T, the antagomir-142-3p attenuated endothelial apoptosis and retarded the atherosclerosis progression in the aorta of ApoE-/- mice [57]
Increase pro-inflammatory cytokines miR-342-5p targets Akt1 induces proinflammatory mediators such as NOS2 and IL-6 in macrophages via the upregulation of miR-155 T, the miR-342-5p antagomir upregulated Akt1 expression and suppressed the expression of miR-155 and NOS2 [58]
Mature plaques          
Marker of response to clopidogrel, targets P2Y12 receptor miR-223-3p possible P2Y12 site targeting on-clopidogrel platelet reactivity decreased miR-223 expression
was a predictor of low responders
to clopidogrel		 [41]
Plaque stabilization miR-145 targets KLF4,5 VSMCs contractility, increase fibrous cap area, reduce the necrotic core area T, delivery of miR-145 may limit atherosclerotic plaque growth, and
restore contractile levels in VSMCs		 [59][60]
Macrophage polarization miR-455 targets SOCS3 decreased expression leads to ECs injury induced by ox-LDL T, overexpression with miR-455
inhibits apoptosis, migration of VSMCs,
and lowers ox-LDL		 [61]
Marker of platelet activation, targets COX-1 receptor through the regulation of TXS miR-34b-3p targets TBXAS1 miR-34b-3p may regulate the platelet response by suppressing TBXAS1 expression and megakaryocyte proliferation T, miR-34b-3p may facilitate the
antiplatelet efficiency of aspirin
through inhibiting TBXAS1		 [62]
Responsive to antiplatelet therapy miR-126-3p affects ADAM9 and P2Y12 receptor expression Increases platelets aggregation T, antagomiR against miR-126-3p reduces platelets aggregation [63]
Decreases size of atherosclerotic lesions, alleviate ox-LDL-induced ECs injury, angiogenesis and vascular integrity miR-126-3p activation of VEGF and NF-kB signaling decreased expression in advanced carotid plaques with high discriminating value (AUC: 0.998) patients with severe carotid stenosis demonstrated down-regulation of miR-126 [64]
Plaque stabilization miR-210 targets the APC gene, affecting Wnt signaling and regulating VSMCs survival enhances fibrous plaque stability in mature plaques T, miR-210 mimics prevent carotid plaque rupture; modulating miR-210 improved
fibrous cap stability		 [65]
Promotes atherosclerosis growth miR-103-3p targets KLF4 stimulates inflammatory activation, and uptake of oxidized LDL cholesterol T, reduction in miR-103 levels results
in the reduction of atherosclerosis
and endothelial inflammation		 [66]
Decreases ECs regeneration and repair miR-652-3p suppression of the endothelial repair gene Ccnd2 inhibits ECs regeneration and repair following mechanical injury downregulates Ccnd2 in endothelial cells, lowering cell proliferation [67]
Plaque stabilization miR-223 targets TLR4 reduces foam cell
formation, and production of pro-inflammatory
cytokines		 Overexpression decreases lipids
deposition and inflammation		 [68]
Plaque instability miR-92a-3p SIRT1, H2O2-induced changes in VSMCs increased apoptosis, oxidative stress, CIMT, and pro-inflammatory MMP-9 miR-92a overexpression regulates
the expression levels of MMP-9
and TIMP3		 [69][70]
Plaque instability miR-133a Matrix metallopeptidase 9 inhibits the proliferation of VSMCs and induces apoptosis the miR-133a-3p mimic inhibited proliferation and promoted VSMC cell apoptosis [71]
Promotes endothelial migration miR-486 targets HAT1 induces apoptosis and oxidative stress, pro-atherosclerotic, affects
endothelial migratory activity		 Inhibition of miR-486 limits foam
cell formation by increasing
cholesterol efflux		 [69][72]
Increases pro-inflammatory cytokines miR-331 down-regulation
of SOCS1		 a pro-inflammatory response in atherosclerotic plaques miR-331 suppression causes up-regulation of SOCS1 and anti-inflammatory mechanism in atherosclerosis [73][74]
Plaque stabilization miR-100 down-regulation of E-selectin and VCAM-1 miR-100 restrains vascular inflammation in vitro and in vivo by suppressing endothelial adhesion molecule expression and thereby attenuating leukocyte–endothelial interaction Inhibition of miR-100 Stimulates Atherogenesis in Mice [75]
Plaque instability miR-105 transported via HDL overexpression of miR-105 in patients with familial hypercholesterolemia HDL can deliver miRNA-105 to recipient cells, contributing to altered gene expression [76]
Plaque instability miR-155 Targets the transcription factor HBP1 Increase macrophages, foam cells content, and necrotic core in plaques T, inhibition of miR-155 reduced necrotic core, apoptosis, and prevented progression of atherosclerosis [77][78]
Plaque instability miR-124 Targets P4HA1 Inhibits collagen synthesis in atherosclerotic plaques Overexpression of miR-124 increased the expression of anti-inflammatory cytokines by binding p38 signaling pathway [79][80]
Plaque instability miR-134 ANGTPL4/LPL associated with chronic inflammation (hs-CRP and TNF-α), cholesterol mass, and plaque vulnerability features on ultrasonography T, lower LPL activity with inhibitors of miR-134 [81][82][83]
Lipometabolism miR-122 inhibits AMPK and SIRT1 correlated with TC, TG, and LDL-C levels serum level of miR-122
correlated with atherosclerosis
severity		 [84]
ABCA1: ATP-binding cassette subfamily A member 1; ABCG1: ATP-binding cassette subfamily G member 1; Akt: protein kinase B; AMPK: Adenosine monophosphate–activated protein kinase; ANG II: angiotensin II; ANGTPL/LPL: Angiopoietin/lipoprotein lipase; Ccnd2: Cyclin D2; CIMT: carotid intima-media thickness; Dlk1: delta-like 1 homolog; eNOS: nitric oxide synthase; ECs: endothelial cells; ET-1: Endothelin 1; H2O2: hydrogen peroxide; HAT1: Histone acetyl-transferase 1; HMG-box transcription factor 1; hs-CRP: high-sensitivity C-Reactive Protein; IGF: insulin growth factor; KLF: Kruppel-like factor; LXRα: Liver X receptor α; LPS: lipopolysaccharide; MAP3K10: mitogen-activated protein 3 kinase 10; MCP-1; monocyte chemotactic protein-1; MMP: metalloproteinase protein; n/d: no data available; NF-κB: nuclear factor-κB; P4HA1: prolyl 4-hydroxylase subunit alpha-1; PPARα: peroxisome proliferators-activated receptor-α, RelA/p65: REL-associated protein involved in NF-κB heterodimer formation p65 subunit; sVEGFR1: soluble VEGF receptor-1; SIRT1: sirtuin 1; SOCS1: suppressor of cytokine signaling 1; T: therapeutic approach; TBXAS1: thromboxane synthase thromboxane A synthase 1; TLR4: toll-like receptor 4; TNF-α: tumor necrosis factor alpha; VCAM-1: vascular cell adhesion molecule-1; VSMC: vascular smooth muscle cells; VEGF: vascular endothelial growth factor.
Some miRs, such as miR-let-7g, also modulate ECs senescence by regulating anti-aging gene sirtuin 1 (SIRT1) and the insulin growth factor (IGF) 1 pathway [42]. In line with this, miR-143 is downregulated with advancing age and protects against vascular senescence [43][44]. On the contrary, miR-92a released from ECs stimulates macrophages to the pro-inflammatory responses and LDL uptake, which enhance atherosclerotic progression [85]. In mice, inhibition of miR-92a reduces endothelial inflammation and atheroma plaque size through the regulation of Kruppel-like factor 2 (KLF2) [47]. Similarly, miR-34a aggravates and accelerates vascular senescence through the downregulation of SIRT1 and AXL Receptor Tyrosine Kinase [48], whereas miR-34a inhibition by anti-miR-34a reduced vascular inflammation, senescence, and apoptosis [49][86]. In macrophages, ox-LDL increases miR-34a levels that target the cholesterol transporters’ ATP-binding cassette subfamily A member 1 (ABCA1), and ATP-binding cassette subfamily G member 1 (ABCG1) [48]. This alters lipid metabolism, while miR-34a enhanced secretion of inflammatory cytokines promotes inflammation facilitating atherosclerotic plaque formation [48][49]. ECs dysregulation is enhanced by the lipid accumulation due to disturbed reverse cholesterol transport of cholesterol efflux from macrophages to the liver [50]. This results in lipid accumulation in macrophages with formation of foam cells [48]. miR-206 and miR-233 promote cholesterol efflux to the liver, whereas miR-33a inhibits reverse transport (Table 1) [39][40][51][87]. miR-33a/b have been shown to act as post-transcriptional regulators of a lipid metabolism, and their pharmacological inhibition diminished atherosclerosis by raising plasma high-density lipoprotein levels [87]. Nguyen et al. demonstrated that chitosan nanoparticles containing miRs can be delivered to macrophages [88]. In mice, macrophages treated with miR-33-loaded nanoparticles showed decreased reverse cholesterol transport [88]. In contrast, when efflux-promoting miRs were delivered the efflux was improved [88].
miR-10a, miR-31, and miR-17-3p regulate inflammation modulating the expression of adhesion molecules in ECs, while miR-155 and miR-331 through the down-regulation of the anti-inflammatory suppressor of cytokine signaling 1 (SOCS1) protein [53][54][73][89][90]. During atherosclerosis development, miR-155 begins to stimulate atherosclerosis progression through repressing Bcl6 in macrophages, suppressing the expression of eNOS, and increasing pro-inflammatory NF-κB signaling [52].
There is a continuous crosstalk between ECs and vascular smooth muscle cells (VSMCs) [91]. ECs-derived miRNAs, like miR-126, miR-92a exert action on VSMCs, resulting in the VSMCs-enriched miRNAs release, that often have reciprocal unfavorable effects on ECs [92][93]. On atherosclerosis initiation, VSCMs migrates from the medial arterial wall into the intimal space, resulting in promotion of plaque formation [91]. VSCMs migration and proliferation is one of key stages in early atherosclerosis. miR-520 regulates VSMCs function by targeting RelA/p65. This way, decreasing cells migration and proliferation exerts a protective role in atherosclerosis [45]. Moreover, miR-520c-3p mimics may act as a promising therapeutic strategy for atherosclerosis [45]. The VSMCs equilibrium plays a great role in the inhibition of atherosclerosis. The maintenance of contractile phenotype prevents atherosclerosis [45][59][60][91][92][93][94]. Of the miRs capable of the contractile function recovery in VSMCs, miR-22 and miR143/145 are probably the most investigated ones, and are potential therapeutic targets [59][60][91][94]. Intravenous delivery of miR-143/145 extracellular vesicles blocked atherosclerotic lesion progression and exerted protective effects on intima-media complex [59][60], while miR-22 restores contractile phenotype of VSMCs without a negative impact on EC’s function [95]. In addition, miR-22 inhibits intima-media hyperplasia, which is important both for inhibition of atherosclerosis plaque growth, as well as in the restenosis following stent implantation [46][95].
Some miRNAs were investigated in the context of carotid plaques, including miR-520, miR-455, and miR-105. Some are common for many arterial territories, including miR-21, miR-27, miR-100, and miR-122 (Table 1) [45][55][56][57][58][61][62][63][64][65][66][67][68][69][70][71][72][74][75][76][77][78][79][80][81][82][83][84][96][97][98][99][100][101][102].
When the anti-atherothrombotic miRNAs are overbalanced by the pro-atherothrombotic miRNAs, researchers can steadily observe carotid intima-media complex thickening (CIMT), followed by the occurrence of focal non-calcified lesions [102]. Then, a formation of mature plaques composed of lipid and necrotic cores, fibrotic matrix, and calcifications are observed, accompanied by inflammation and angiogenesis. The first caution that should attract the attention of clinicians is CIMT [103][104][105]. CIMT, in ranges above the 75th percentile for age and gender, can even be observed in teenagers and young adults, particularly if accompanied by atherosclerosis risk factors, such as diabetes or familial hypercholesterolemia [106][107]. This parameter is well correlated with risk of cardiovascular events, such as cardiovascular death (CVD), IS, and myocardial infarction (MI) [103][104][105]. It has also a good predictive value for a presence of significant atherosclerosis in the other territories, e.g., coronary arteries [108][109]. Several miRNAs are associated with CIMT, including miR-22, miR-29a, miR-143/145, and miR-92a [46][70][110][111]. With increasing CIMT, atherosclerotic process accelerates. There is a huge role for metalloproteinases (MMP), such as MMP-2 and MMP-9, as they are associated with a promotion of plaque growth and CIMT increase, rather than a decrease in VSMCs contractility [111]. Interestingly, in advanced carotid plaques, migration and proliferation of VSMCs is beneficial, promoting the stability of the fibrous cap and prevention of plaque rupture [91][102]. This process in stimulated by the expression of miR-145 and miR-210 that drive the increase in plaque collagen content and a fibrous cap area, while at the same time reducing the necrotic core area [46][65][95].
In contrast, plaque instability is associated with increasing levels of MMP-2, MMP-9, the increasing size of plaque and the lipid and necrotic core, particularly when abundant in lipids [111][112][113][114]. MMP-9 is particularly important as it predicts future adverse cardiovascular events [71][111][112][113]. It was observed that MMP-9 is regulated by several miRNAs, including miR-92a, which is a predictor of plaque instability [114]. However, miR-92a is not necessarily always negative [115][116]. The upregulation of MMP-9 and the downregulation of TIMP3 in H2O2-induced VSMCs were observed to be reversed by mimicking miR-92a in addition to SIRT1 and siRNA, which may prevent a phenotypic change of VSMCs [115][116]. Other miRNAs associated with serum concentration of MMP-9 include miR-100, miR-155, miR-133a, and miR-223 [111][114]. These miRNAs are also linked to plaque instability and might be used as biomarkers of plaque conversion from a stable state into a vulnerable state [114][115][116][117][118][119].
Thus, it is of the utmost importance to identify carotid plaques that are likely to undergo transformation from the stable ones to vulnerable ones, prone to rupture and cause symptoms of cerebral ischemia. The research is ongoing for the identification of specific microRNAs that could prevent IS through the manipulation of their expression levels.

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Subjects: Medicine, Research & Experimental
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : Rafał Badacz ,
Tadeusz Przewłocki
, Jacek Legutko ,
Krzysztof Żmudka
, Anna Kabłak-Ziembicka
View Times: 508
Revisions: 2 times (View History)
Update Date: 19 Dec 2022
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