microRNAs Associated with Carotid Plaque Development and Vulnerability: The Clinician’s Perspective

Badacz, Rafał; Przewłocki, Tadeusz; Legutko, Jacek; Żmudka, Krzysztof; Kabłak‐Ziembicka, Anna

doi:10.3390/ijms232415645

Cited by 19 publications

(17 citation statements)

References 152 publications

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“…26 For example, miR-126, miR-155, miR-206, and miR-223 prevent unfavourable lipid metabolism and reduce inflammation via many signalling pathways; other miRs, such as miR-let-7g, miR-143, and miR-34a, modulate endothelial cell senescence by regulating related protein; also, miR-10a, miR-31, and miR-17-3p regulate inflammation by modulating the expression of adhesion molecules. 27 Most recently, miR-22-3p has been reported to inhibit human aortic SMC proliferation and migration, affecting vascular pathologies. 17 However, the mechanism of miR-22-3p has not been fully explored in AS.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-22-3p alleviates atherosclerosis by mediating macrophage M2 polarization as well as inhibiting NLRP3 activation

Bian,

Peng,

Wang

et al. 2023

J Int Med Res

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Objective MicroRNA (miR)-22-3p is expressed in atherosclerosis (AS), but its function and regulatory mechanisms remain unclear. Therefore, the effects of miR-22-3p in AS were assessed in this study. Methods MiR-22-3p expression was assessed in AS, and miR-22-3p target genes were predicted using sequencing transcriptomics. The effect of miR-22-3p agomir on atherosclerotic lesions in an AS mouse model were determined by Oil red O, Masson’s, and sirius red staining, and by anti-smooth muscle actin and macrophage antigen-3 immunostaining. Gene expression in AS was evaluated by western blot and immunofluorescence. Results MiR-22-3p was expressed in AS and control samples (32.5% and 33.9% levels, respectively, relative to total miRNA among six highly expressed miRNAs). In the mouse model of AS, miR-22-3p agomir significantly reduced lipid deposition, proliferation of aortic collagen fibres, and macrophage content. Additionally, inducible nitric oxide synthase, interleukin-6, and tumour necrosis factor-α levels were significantly reduced, and levels of arginase 1 and CD206 were significantly enhanced. MiR-22-3p was found to target janus kinase 1( JAK1), and significantly inhibited the activation of NLR family pyrin domain containing 3 (NLRP3) and JAK1 in mice. Conclusions MiR-22-3p appears to reduce the inflammatory response in AS, which might be achieved by inducing the M2 macrophage phenotype and suppressing NLRP3 activation via JAK1.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-22-3p alleviates atherosclerosis by mediating macrophage M2 polarization as well as inhibiting NLRP3 activation

Bian,

Peng,

Wang

et al. 2023

J Int Med Res

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“…Early atherosclerotic lesions begin with lipid infiltrates and are highly dynamic lesions containing inflammatory cells (monocytes, leukocytes, and macrophages); inflammatory cytokines (interleukins such as IL-1β and IL-6; tumor necrosis and growth factors such as TNF-α and TGF-β1; and metalloproteinases such as MMP-2 and MMP-9); oxidation products (e.g., oxy-LDL cholesterol); and in diabetic patients, glycation products [ 34 , 37 ]. Atherosclerosis is not solely initiated by atherogenic lipoproteins such as Lp(a), LDL, IDL, or VRDL, but also by genetic factors, such as short non-coding nucleotide sequences of microRNAs [ 37 , 38 , 39 , 40 , 41 ]. These microRNAs play a role in the regulation of all metabolic pathways through the selective blocking of mRNA, which then affects the production of proteins and enzymes [ 42 ].…”

Section: The Faces Of Atherosclerosismentioning

confidence: 99%

A Non-Coronary, Peripheral Arterial Atherosclerotic Disease (Carotid, Renal, Lower Limb) in Elderly Patients—A Review: Part I—Epidemiology, Risk Factors, and Atherosclerosis-Related Diversities in Elderly Patients

Piechocki,

Przewłocki,

Pieniążek

et al. 2024

JCM

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Atherosclerosis is a generalized and progressive disease. Ageing is a key risk factor for atherosclerosis progression that is associated with the increased incidence of ischemic events in supplied organs, including stroke, coronary events, limb ischemia, or renal failure. Cardiovascular disease is the leading cause of death and major disability in adults ≥ 75 years of age. Atherosclerotic occlusive disease affects everyday activity and quality of life, and it is associated with reduced life expectancy. Although there is evidence on coronary artery disease management in the elderly, there is insufficient data on the management in older patients presented with atherosclerotic lesions outside the coronary territory. Despite this, trials and observational studies systematically exclude older patients, particularly those with severe comorbidities, physical or cognitive dysfunctions, frailty, or residence in a nursing home. This results in serious critical gaps in knowledge and a lack of guidance on the appropriate medical treatment and referral for endovascular or surgical interventions. Therefore, we attempted to gather data on the prevalence, risk factors, and management strategies in patients with extra-coronary atherosclerotic lesions.

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“…The second approach involves early intervention at the level of atherosclerotic growth initiation [4,5,74]. The optimal point for early intervention would be during the identification of intima-media complex thickening or the presence of early plaques [127][128][129].…”

Section: Future Directions and Conclusionmentioning

confidence: 99%

“…Atherosclerosis initiation and progression are driven by multiple pro-inflammatory and pro-thrombotic microRNAs that overcome micro-RNAs with protective functions against atherosclerosis [4][5][6]. Atherosclerotic plaque rupture is the leading cause of cardiovascular death resulting from acute coronary syndromes (ACS), both in ST-segment (STEMI) and non-ST segment elevation (NSTEMI) myocardial infarction, as well as cardiac remodeling and fibrosis following ACS [4][5][6].…”

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confidence: 99%

Cardiac microRNAs: diagnostic and therapeutic potential

Kabłak-Ziembicka,

Badacz,

Okarski

et al. 2023

Arch Med Sci

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MicroRNAs are small non-coding post-translational biomolecules which, when expressed, modify their target genes. It is estimated that microRNAs regulate production of approximately 60% of all human proteins and enzymes that are responsible for major physiological processes. In cardiovascular disease pathophysiology, there are several cells that produce microRNAs, including endothelial cells, vascular smooth muscle cells, macrophages, platelets, and cardiomyocytes. There is a constant crosstalk between microRNAs derived from various cell sources. Atherosclerosis initiation and progression are driven by many pro-inflammatory and pro-thrombotic microRNAs. Atherosclerotic plaque rupture is the leading cause of cardiovascular death resulting from acute coronary syndrome (ACS) and leads to cardiac remodeling and fibrosis following ACS. MicroRNAs are powerful modulators of plaque progression and transformation into a vulnerable state, which can eventually lead to plaque rupture. There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. Understanding their mechanisms may lead to the development of microRNA cocktails that can potentially be used in regenerative cardiology.

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microRNAs Associated with Carotid Plaque Development and Vulnerability: The Clinician’s Perspective

Cited by 19 publications

References 152 publications

MicroRNA-22-3p alleviates atherosclerosis by mediating macrophage M2 polarization as well as inhibiting NLRP3 activation

MicroRNA-22-3p alleviates atherosclerosis by mediating macrophage M2 polarization as well as inhibiting NLRP3 activation

A Non-Coronary, Peripheral Arterial Atherosclerotic Disease (Carotid, Renal, Lower Limb) in Elderly Patients—A Review: Part I—Epidemiology, Risk Factors, and Atherosclerosis-Related Diversities in Elderly Patients

Cardiac microRNAs: diagnostic and therapeutic potential

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