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      Inflammatory microRNAs in cardiovascular pathology: another brick in the wall

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          Abstract

          The regulatory role of microRNAs (miRNAs) is mainly mediated by their effect on protein expression and is recognized in a multitude of pathophysiological processes. In recent decades, accumulating evidence has interest in these factors as modulatory elements of cardiovascular pathophysiology. Furthermore, additional biological processes have been identified as new components of cardiovascular disease etiology. In particular, inflammation is now considered an important cardiovascular risk factor. Thus, in the present review, we will focus on the role of a subset of miRNAs called inflamma-miRs that may regulate inflammatory status in the development of cardiovascular pathology. According to published data, the most representative candidates that play functional roles in thromboinflammation are miR-21, miR-33, miR-34a, miR-146a, miR-155, and miR-223. We will describe the functions of these miRNAs in several cardiovascular pathologies in depth, with specific emphasis on the molecular mechanisms related to atherogenesis. We will also discuss the latest findings on the role of miRNAs as regulators of neutrophil extracellular traps and their impact on cardiovascular diseases. Overall, the data suggest that the use of miRNAs as therapeutic tools or biomarkers may improve the diagnosis or prognosis of adverse cardiovascular events in inflammatory diseases. Thus, targeting or increasing the levels of adequate inflamma-miRs at different stages of disease could help mitigate or avoid the development of cardiovascular morbidities.

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          Most cited references138

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          Neutrophil extracellular traps kill bacteria.

          Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.
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            Metazoan MicroRNAs

            MicroRNAs (miRNAs) are ∼22 nt RNAs that direct posttranscriptional repression of mRNA targets in diverse eukaryotic lineages. In humans and other mammals, these small RNAs help sculpt the expression of most mRNAs. This article reviews advances in our understanding of the defining features of metazoan miRNAs and their biogenesis, genomics, and evolution. It then reviews how metazoan miRNAs are regulated, how they recognize and cause repression of their targets, and the biological functions of this repression, with a compilation of knockout phenotypes that shows that important biological functions have been identified for most of the broadly conserved miRNAs of mammals.
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              Atherosclerosis — An Inflammatory Disease

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                Author and article information

                Contributors
                URI : https://loop.frontiersin.org/people/1203029
                URI : https://loop.frontiersin.org/people/1023998
                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                18 May 2023
                2023
                : 14
                : 1196104
                Affiliations
                [1] Department of Hematology, Morales Meseguer University Hospital, Centro Regional de Hemodonación, Universidad de Murcia, IMIB Pascual Parrilla , Murcia, Spain
                Author notes

                Edited by: Guo-Chang Fan, University of Cincinnati, United States

                Reviewed by: Harish Palleti Janardhan, University of Massachusetts Medical School, United States; Jingbo Pang, University of Illinois Chicago, United States

                *Correspondence: Constantino Martínez, constant@ 123456um.es ; Rocío González-Conejero, rocio.gonzalez@ 123456carm.es

                †These authors share senior authorship

                Article
                10.3389/fimmu.2023.1196104
                10233054
                c02f8afd-c7f7-49f2-b193-8c8c98b52dcd
                Copyright © 2023 Zapata-Martínez, Águila, de los Reyes-García, Carrillo-Tornel, Lozano, González-Conejero and Martínez

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 29 March 2023
                : 08 May 2023
                Page count
                Figures: 1, Tables: 2, Equations: 0, References: 138, Pages: 14, Words: 8660
                Funding
                Funded by: Instituto de Salud Carlos III , doi 10.13039/501100004587;
                This work was supported by research grants from Instituto de Salud Carlos III (ISCIII), Fondo Europeo de Desarrollo Regional “Investing in your future” (PI20/00136) (FI21/00065: LZ-M), (CP21/00053: SA) (PFIS18/0045: AR-G), and Sociedad Española de Trombosis y Hemostasia (SETH).
                Categories
                Immunology
                Review
                Custom metadata
                Inflammation

                Immunology
                micrornas,cardiovascular diseases,inflammation,neutrophil extracellular traps (net),thromboinflammation

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