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Non Coding RNA in Cardiovascular Biology and Medicine

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 31964

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Special Issue Editors

Prof. Dr. Constanza Emanueli

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Guest Editor

National Heart and Lung Institute, Imperial College London, Hammersmith Campus, London W12 0NN, UK
Interests: regulatory RNAs; extracellular vesicles; therapeutic angiogenesis; diabetes and ischemic disease

Dr. Susana Novella

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Guest Editor

1. Department of Physiology, University of Valencia, 46010 Valencia, Spain
2. INCLIVA Biomedical Research Institute, Valencia, Spain
Interests: estradiol; aging; miRNA; endothelium; sex differences; cardiovascular physiology

Prof. Dr. Rajesh Katare

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Department of Physiology, HeartOtago, University of Otago School of Biomedical Sciences, Dunedin, New Zealand
Interests: diabetic heart disease; microRNAs; stem cells; chronic ischemia; diabetic foot
Special Issues, Collections and Topics in MDPI journals

Dr. Miron Sopić

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Department of Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia
Interests: lncRNAs; microRNAs; cell-free RNAs; liquid biopsy; cardiometabolic diseases; inflammaging

Special Issue Information

Dear Colleagues,

Despite the progress in diagnosis and management of cardiovascular diseases, heart disease is still the killer number one, and vascular disease is involved in a plethora of severe conditions outside the heart, from vascular dementia and stroke to pulmonary atherosclerosis, critical limb ischemia, diabetic retinopathy and nephropathy, and so forth.

Current clinical strategies still rely on the use of traditional risk factors and conclusions drawn from population studies. However, most cardiovascular events occur in patients with one or few traditional risk factors, whereas some individuals classified as high risk never experience clinical events. This high risk is usually along with aging due to the increased burden of comorbidities and is furthermore more evident in women as they also face the physiological changes caused by menopause. Social inequality and ethnical differences can also increase cardiovascular risks. It is evident that we need to go beyond and above traditional risk factors in order to identify novel pathophysiological players related to the development and progression of cardiovascular disease, which can translate into more efficient and personalized therapeutic targets. These newly identified targets should be transferred from bench to bedside and implemented into novel, more male and female patient-oriented, diagnostic, prognostic, and therapeutic strategies.

The technological advancements in recent decades have revolutionized our understanding of the human genome and epigenome, allowing to unravel the prevalence of noncoding RNA species, with important regulatory roles, and the importance of multilayer regulatory mechanisms such as DNA and RNA methylation. While basic research continues to push the boundaries with new discoveries on the complexity of the RNA world, several classes of noncoding RNAs such as microRNAs, long noncoding RNAs, and circular RNAs have already shown their translational potential as cardiovascular biomarkers and therapeutic targets. With the latest advancements in the development of RNA-based vaccines, and RNA-interfering drugs such as Inclisiran for the treatment of heterozygous familial hypercholesterolemia, it is expected that the RNA therapeutics field will progress even more rapidly.

This Special Issue of Cells is proposed by members of the European CardioRNA COST Action initiative (CA17129—Catalysing transcriptomics research in cardiovascular disease; www.cardiorna.eu), which aims to emphasize discoveries related to the novel functions of noncoding RNAs in the development and progression of cardiovascular diseases, as well as the development of novel RNA-based diagnostic and therapeutic tools.

Prof. Dr. Constanza Emanueli
Dr. Susana Novella
Prof. Dr. Rajesh Katare
Dr. Miron Sopić
Guest Editors

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Keywords

lncRNA
miRNA
circRNA
cardiovascular disease
atherosclerosis
biomarkers
epitrasncriptomics
RNA editing

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Research

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17 pages, 2516 KiB

Open AccessArticle

A Segmental Approach from Molecular Profiling to Medical Imaging to Study Bicuspid Aortic Valve Aortopathy

by Froso Sophocleous, Estefania De Garate, Maria Giulia Bigotti, Maryam Anwar, Eva Jover, Aranzazu Chamorro-Jorganes, Cha Rajakaruna, Konstantina Mitrousi, Viola De Francesco, Aileen Wilson, Serban Stoica, Andrew Parry, Umberto Benedetto, Pierpaolo Chivasso, Frances Gill, Mark C. K. Hamilton, Chiara Bucciarelli-Ducci, Massimo Caputo, Costanza Emanueli and Giovanni Biglino

Cells 2022, 11(23), 3721; https://doi.org/10.3390/cells11233721 - 22 Nov 2022

Cited by 1 | Viewed by 2090

Abstract

Bicuspid aortic valve (BAV) patients develop ascending aortic (AAo) dilation. The pathogenesis of BAV aortopathy (genetic vs. haemodynamic) remains unclear. This study aims to identify regional changes around the AAo wall in BAV patients with aortopathy, integrating molecular data and clinical imaging. BAV patients with aortopathy (n = 15) were prospectively recruited to surgically collect aortic tissue and measure molecular markers across the AAo circumference. Dilated (anterior/right) vs. non-dilated (posterior/left) circumferential segments were profiled for whole-genomic microRNAs (next-generation RNA sequencing, miRCURY LNA PCR), protein content (tandem mass spectrometry), and elastin fragmentation and degeneration (histomorphometric analysis). Integrated bioinformatic analyses of RNA sequencing and proteomic datasets identified five microRNAs (miR-128-3p, miR-210-3p, miR-150-5p, miR-199b-5p, and miR-21-5p) differentially expressed across the AAo circumference. Among them, three miRNAs (miR-128-3p, miR-150-5p, and miR-199b-5p) were predicted to have an effect on eight common target genes, whose expression was dysregulated, according to proteomic analyses, and involved in the vascular-endothelial growth-factor signalling, Hippo signalling, and arachidonic acid pathways. Decreased elastic fibre levels and elastic layer thickness were observed in the dilated segments. Additionally, in a subset of patients n = 6/15, a four-dimensional cardiac magnetic resonance (CMR) scan was performed. Interestingly, an increase in wall shear stress (WSS) was observed at the anterior/right wall segments, concomitantly with the differentially expressed miRNAs and decreased elastic fibres. This study identified new miRNAs involved in the BAV aortic wall and revealed the concomitant expressional dysregulation of miRNAs, proteins, and elastic fibres on the anterior/right wall in dilated BAV patients, corresponding to regions of elevated WSS. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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16 pages, 6495 KiB

Open AccessArticle

CircANKRD12 Is Induced in Endothelial Cell Response to Oxidative Stress

by Christine Voellenkle, Paola Fuschi, Martina Mutoli, Matteo Carrara, Paolo Righini, Giovanni Nano, Carlo Gaetano and Fabio Martelli

Cells 2022, 11(22), 3546; https://doi.org/10.3390/cells11223546 - 9 Nov 2022

Cited by 5 | Viewed by 2507

Abstract

Redox imbalance of the endothelial cells (ECs) plays a causative role in a variety of cardiovascular diseases. In order to better understand the molecular mechanisms of the endothelial response to oxidative stress, the involvement of circular RNAs (circRNAs) was investigated. CircRNAs are RNA species generated by a “back-splicing” event, which is the covalent linking of the 3′- and 5′-ends of exons. Bioinformatics analysis of the transcriptomic landscape of human ECs exposed to H₂O₂ allowed us to identify a subset of highly expressed circRNAs compared to their linear RNA counterparts, suggesting a potential biological relevance. Specifically, circular Ankyrin Repeat Domain 12 (circANKRD12), derived from the junction of exon 2 and exon 8 of the ANKRD12 gene (hsa_circ_0000826), was significantly induced in H₂O₂-treated ECs. Conversely, the linear RNA isoform of ANKRD12 was not modulated. An increased circular-to-linear ratio of ANKRD12 was also observed in cultured ECs exposed to hypoxia and in skeletal muscle biopsies of patients affected by critical limb ischemia (CLI), two conditions associated with redox imbalance and oxidative stress. The functional relevance of circANKRD12 was shown by the inhibition of EC formation of capillary-like structures upon silencing of the circular but not of the linear isoform of ANKRD12. Bioinformatics analysis of the circANKRD12–miRNA–mRNA regulatory network in H₂O₂-treated ECs identified the enrichment of the p53 and Foxo signaling pathways, both crucial in the cellular response to redox imbalance. In keeping with the antiproliferative action of the p53 pathway, circANKRD12 silencing inhibited EC proliferation. In conclusion, this study indicates circANKRD12 as an important player in ECs exposed to oxidative stress. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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14 pages, 535 KiB

Open AccessArticle

Identifying Candidate Circulating RNA Markers for Coronary Artery Disease by Deep RNA-Sequencing in Human Plasma

by Zoe Ward, Sebastian Schmeier, John Pearson, Vicky A Cameron, Chris M Frampton, Richard W Troughton, Rob N Doughty, A. Mark Richards and Anna P Pilbrow

Cells 2022, 11(20), 3191; https://doi.org/10.3390/cells11203191 - 11 Oct 2022

Cited by 10 | Viewed by 3571

Abstract

Advances in RNA sequencing (RNA-Seq) have facilitated transcriptomic analysis of plasma for the discovery of new diagnostic and prognostic markers for disease. We aimed to develop a short-read RNA-Seq protocol to detect mRNAs, long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in plasma for the discovery of novel markers for coronary artery disease (CAD) and heart failure (HF). Circulating cell-free RNA from 59 patients with stable CAD (half of whom developed HF within 3 years) and 30 controls was sequenced to a median depth of 108 paired reads per sample. We identified fragments from 3986 messenger RNAs (mRNAs), 164 long non-coding RNAs (lncRNAs), 405 putative novel lncRNAs and 227 circular RNAs in plasma. Circulating levels of 160 mRNAs, 10 lncRNAs and 2 putative novel lncRNAs were altered in patients compared with controls (absolute fold change >1.2, p < 0.01 adjusted for multiple comparisons). The most differentially abundant transcripts were enriched in mRNAs encoded by the mitochondrial genome. We did not detect any differences in the plasma RNA profile between patients who developed HF compared with those who did not. In summary, we show that mRNAs, lncRNAs and circular RNAs can be reliably detected in plasma by deep RNA-Seq. Multiple coding and non-coding transcripts were altered in association with CAD, including several mitochondrial mRNAs, which may indicate underlying myocardial ischaemia and oxidative stress. If validated, circulating levels of these transcripts could potentially be used to help identify asymptomatic individuals with established CAD prior to an acute coronary event. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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20 pages, 3620 KiB

Open AccessArticle

In Vivo Inhibition of miR-34a Modestly Limits Cardiac Enlargement and Fibrosis in a Mouse Model with Established Type 1 Diabetes-Induced Cardiomyopathy, but Does Not Improve Diastolic Function

by Bianca C. Bernardo, Gunes S. Yildiz, Helen Kiriazis, Claudia A. Harmawan, Celeste M. K. Tai, Rebecca H. Ritchie and Julie R. McMullen

Cells 2022, 11(19), 3117; https://doi.org/10.3390/cells11193117 - 3 Oct 2022

Cited by 8 | Viewed by 3078

Abstract

MicroRNA 34a (miR-34a) is elevated in the heart in a setting of cardiac stress or pathology, and we previously reported that inhibition of miR-34a in vivo provided protection in a setting of pressure overload-induced pathological cardiac hypertrophy and dilated cardiomyopathy. Prior work had also shown that circulating or cardiac miR-34a was elevated in a setting of diabetes. However, the therapeutic potential of inhibiting miR-34a in vivo in the diabetic heart had not been assessed. In the current study, type 1 diabetes was induced in adult male mice with 5 daily injections of streptozotocin (STZ). At 8 weeks post-STZ, when mice had established type 1 diabetes and diastolic dysfunction, mice were administered locked nucleic acid (LNA)-antimiR-34a or saline-control with an eight-week follow-up. Cardiac function, cardiac morphology, cardiac fibrosis, capillary density and gene expression were assessed. Diabetic mice presented with high blood glucose, elevated liver and kidney weights, diastolic dysfunction, mild cardiac enlargement, cardiac fibrosis and reduced myocardial capillary density. miR-34a was elevated in the heart of diabetic mice in comparison to non-diabetic mice. Inhibition of miR-34a had no significant effect on diastolic function or atrial enlargement, but had a mild effect on preventing an elevation in cardiac enlargement, fibrosis and ventricular gene expression of B-type natriuretic peptide (BNP) and the anti-angiogenic miRNA (miR-92a). A miR-34a target, vinculin, was inversely correlated with miR-34a expression, but other miR-34a targets were unchanged. In summary, inhibition of miR-34a provided limited protection in a mouse model with established type 1 diabetes-induced cardiomyopathy and failed to improve diastolic function. Given diabetes represents a systemic disorder with numerous miRNAs dysregulated in the diabetic heart, as well as other organs, strategies targeting multiple miRNAs and/or earlier intervention is likely to be required. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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17 pages, 5315 KiB

Open AccessArticle

Hydrogen Sulfide Improves Angiogenesis by Regulating the Transcription of pri-miR-126 in Diabetic Endothelial Cells

by Wenlong Xue, Qingqing Zhang, Ying Chen and Yichun Zhu

Cells 2022, 11(17), 2651; https://doi.org/10.3390/cells11172651 - 25 Aug 2022

Cited by 20 | Viewed by 2820

Abstract

Introduction: Diabetes mellitus results in high rates of cardiovascular disease, such as microcirculation disorder of the lower limbs, with angiogenesis impairment being the main factor. The endothelium functions as a barrier between blood and the vessel wall. Vascular endothelial cell dysfunction caused by hyperglycemia is the main factor leading to angiogenesis impairment. Hydrogen sulfide (H₂S) and miR-126-3p are known for their pro-angiogenesis effects; however, little is known about how H₂S regulates miR-126-3p to promote angiogenesis under high-glucose conditions. Objectives: The main objective of this research was to explore how H₂S regulates the miR-126-3p levels under high-glucose conditions. Methods: We evaluated the pro-angiogenesis effects of H₂S in the diabetic hindlimb of an ischemia mice model and in vivo Matrigel plugs. Two microRNA datasets were used to screen microRNAs regulated by both diabetes and H₂S. The mRNA and protein levels were detected through real-time PCR and Western blot, respectively. Immunofluorescent staining was also used to assess the capillary density and to evaluate the protein levels in vascular endothelial cells. Human umbilical vein endothelial cells (HUVECs) were used in in vitro experiments. A scratch wound-healing assay was applied to detect the migration ability of endothelial cells. Methylated DNA immunoprecipitation combined with real-time PCR was chosen to identify the DNA methylation level in the HUVECs. Results: Exogenous H₂S improved angiogenesis in diabetic mice. miR-126-3p was regulated by both diabetes and H₂S. Exogenous H₂S up-regulated the miR-126-3p level and recovered the migration rate of endothelial cells via down-regulating the DNMT1 protein level, which was increased by high glucose. Furthermore, DNMT1 upregulation in the HUVECs increased the methylation levels of the gene sequences upstream of miR-126-3p and then inhibited the transcription of primary-miR-126, thus decreasing the miR-126-3p level. CSE overexpression in the HUVECs rescued the miR-126-3p level, by decreasing the methylation level to improve migration. Conclusion: H₂S increases the miR-126-3p level through down-regulating the methylation level, by decreasing the DNMT1 protein level induced by high glucose, thus improving the angiogenesis originally impaired by high glucose. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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12 pages, 1902 KiB

Open AccessArticle

Regulation of N6-Methyladenosine after Myocardial Infarction

by Mélanie Vausort, Magdalena Niedolistek, Andrew I. Lumley, Marta Oknińska, Aleksandra Paterek, Michał Mączewski, Xiangyi Dong, Christian Jäger, Carole L. Linster, Przemyslaw Leszek and Yvan Devaux

Cells 2022, 11(15), 2271; https://doi.org/10.3390/cells11152271 - 22 Jul 2022

Cited by 14 | Viewed by 3057

Abstract

Development of heart failure (HF) after myocardial infarction (MI) is responsible for premature death. Complex cellular and molecular mechanisms are involved in this process. A number of studies have linked the epitranscriptomic RNA modification N6-methyladenosine (m6A) with HF, but it remains unknown how m6A affects the risk of developing HF after MI. We addressed the regulation of m6A and its demethylase fat mass and obesity-associated (FTO) after MI and their association with HF. Using liquid chromatography coupled to mass spectrometry, we observed an increase of m6A content in the infarcted area of rat hearts subjected to coronary ligation and a decrease in blood. FTO expression measured by quantitative PCR was downregulated in the infarcted hearts. In whole blood samples collected at the time of reperfusion in MI patients, m6A content was lower in patients who developed HF as attested by a 4-month ejection fraction (EF) of ≤40% as compared to patients who did not develop HF (EF > 50%). M6A content was higher in females. These results show that m6A measured in blood is associated with HF development after MI and motivate further investigation of the potential role of m6A as a novel epitranscriptomics biomarker and therapeutic target of HF. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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19 pages, 3149 KiB

Open AccessArticle

Circulating miRNA Fingerprint and Endothelial Function in Myocardial Infarction: Comparison at Acute Event and One-Year Follow-Up

by Ana Mompeón, Daniel Pérez-Cremades, Ana Belén Paes, Juan Sanchis, Luis Ortega-Paz, Rut Andrea, Salvatore Brugaletta, Manel Sabate, Susana Novella, Ana Paula Dantas and Carlos Hermenegildo

Cells 2022, 11(11), 1823; https://doi.org/10.3390/cells11111823 - 2 Jun 2022

Cited by 11 | Viewed by 2958

Abstract

MicroRNAs (miRNA) are major regulators of intercellular communication and key players in the pathophysiology of cardiovascular disease. This study aimed to determine the miRNA fingerprint in a cohort of 53 patients with acute myocardial infarction (AMI) with non-ST-segment elevation (NSTEMI) relative to miRNA expression in healthy controls (n = 51). miRNA expression was initially profiled by miRNA array in the serum of patients undergoing cardiac catheterization during NSTEMI (n = 8) and 1 year past the event (follow-up, n = 8) and validated in the entire cohort. In total, 58 miRNAs were differentially expressed during AMI (p < 0.05), while 36 were modified at follow-up (Fisher’s exact test: p = 0.0138). Enrichment analyses revealed differential regulation of biological processes by miRNA at each specific time point (AMI vs. follow-up). During AMI, the miRNA profile was associated mainly with processes involved in vascular development. However, 1 year after AMI, changes in miRNA expression were partially related to the regulation of cardiac tissue morphogenesis. Linear correlation analysis of miRNA with serum levels of cytokines and chemokines revealed that let-7g-5p, let-7e-5p, and miR-26a-5p expression was inversely associated with serum levels of pro-inflammatory cytokines TNF-α, and the chemokines MCP-3 and MDC. Transient transfection of human endothelial cells (HUVEC) with let-7e-5p inhibitor or mimic demonstrated a key role for this miRNA in endothelial function regulation in terms of cell adhesion and angiogenesis capacity. HUVEC transfected with let-7e-5p mimic showed a 20% increase in adhesion capacity, whereas transfection with let-7e-5p inhibitor increased the number of tube-like structures. This study pinpoints circulating miRNA expression fingerprint in NSTEMI patients, specific to the acute event and changes at 1-year follow-up. Additionally, given its involvement in modulating endothelial cell function and vascularization, altered let-7e-5p expression may constitute a therapeutic biomarker and target for ischemic heart disease. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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26 pages, 7581 KiB

Open AccessArticle

Comprehensive Characterization of Platelet-Enriched MicroRNAs as Biomarkers of Platelet Activation

by Teresa L. Krammer, Stephan Zeibig, Waltraud C. Schrottmaier, Anita Pirabe, Silvia Goebel, Andreas B. Diendorfer, Hans-Peter Holthoff, Alice Assinger and Matthias Hackl

Cells 2022, 11(8), 1254; https://doi.org/10.3390/cells11081254 - 7 Apr 2022

Cited by 16 | Viewed by 3782

Abstract

Dysregulation of platelet function is causally connected to thrombus formation and cardiovascular diseases. Therefore, assessing platelet reactivity is crucial. However, current platelet function tests come with pitfalls, limiting clinical use. Plasma miRNA signatures have been suggested as novel biomarkers for predicting/diagnosing cardiovascular diseases and monitoring antiplatelet therapy. Here, we provide results from a comprehensive study on the feasibility of using circulatory platelet miRNAs as surrogate markers of platelet activation. We performed small RNA-Seq on different blood cell types to confirm known and identify novel platelet-enriched miRNAs and validated a panel of 16 miRNAs using RT-qPCR. To identify the main carrier of these blood-based platelet miRNAs, we enriched and analyzed distinct microvesicle populations. Platelets were stimulated with GPVI and P2Y12 agonists in vitro to monitor the release of the selected miRNAs following activation. Finally, the miRNA panel was also measured in plasma from mice undergoing the Folts intervention (recurrent thrombus formation in the carotid artery). Applying an unbiased bioinformatics-supported workflow to our NGS data, we were able to confirm a panel of previously established miRNA biomarker candidates and identify three new candidates (i.e., miR-199a-3p, miR-151a-5p, and miR-148b-3p). Basal levels of platelet-derived miRNAs in plasma were mainly complexed with proteins, not extracellular vesicles. We show that changes in miRNA levels due to platelet activation are detectable using RT-qPCR. In addition, we highlight limitations of studying the in vitro release of miRNAs from platelets. In vivo thrombosis resulted in significant elevations of platelet-derived miRNA levels in mice. In conclusion, we provide in-depth evidence that activated platelets release miRNAs, resulting in measurable changes in circulatory miRNA levels, rendering them promising biomarker candidates. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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Review

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20 pages, 2065 KiB

Open AccessReview

LncRNAs as Regulators of Atherosclerotic Plaque Stability

by Aleksa Petkovic, Sanja Erceg, Jelena Munjas, Ana Ninic, Sandra Vladimirov, Aleksandar Davidovic, Luka Vukmirovic, Marko Milanov, Dane Cvijanovic, Tijana Mitic and Miron Sopic

Cells 2023, 12(14), 1832; https://doi.org/10.3390/cells12141832 - 12 Jul 2023

Cited by 6 | Viewed by 2692

Abstract

Current clinical data show that, despite constant efforts to develop novel therapies and clinical approaches, atherosclerotic cardiovascular diseases (ASCVD) are still one of the leading causes of death worldwide. Advanced and unstable atherosclerotic plaques most often trigger acute coronary events that can lead to fatal outcomes. However, despite the fact that different plaque phenotypes may require different treatments, current approaches to prognosis, diagnosis, and classification of acute coronary syndrome do not consider the diversity of plaque phenotypes. Long non-coding RNAs (lncRNAs) represent an important class of molecules that are implicated in epigenetic control of numerous cellular processes. Here we review the latest knowledge about lncRNAs’ influence on plaque development and stability through regulation of immune response, lipid metabolism, extracellular matrix remodelling, endothelial cell function, and vascular smooth muscle function, with special emphasis on pro-atherogenic and anti-atherogenic lncRNA functions. In addition, we present current challenges in the research of lncRNAs’ role in atherosclerosis and translation of the findings from animal models to humans. Finally, we present the directions for future lncRNA-oriented research, which may ultimately result in patient-oriented therapeutic strategies for ASCVD. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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31 pages, 2124 KiB

Open AccessReview

Clinical Significance of MicroRNAs, Long Non-Coding RNAs, and CircRNAs in Cardiovascular Diseases

by Desh Deepak Singh, Youngsun Kim, Seung Ah Choi, Ihn Han and Dharmendra Kumar Yadav

Cells 2023, 12(12), 1629; https://doi.org/10.3390/cells12121629 - 14 Jun 2023

Cited by 24 | Viewed by 3615

Abstract

Based on recent research, the non-coding genome is essential for controlling genes and genetic programming during development, as well as for health and cardiovascular diseases (CVDs). The microRNAs (miRNAs), lncRNAs (long ncRNAs), and circRNAs (circular RNAs) with significant regulatory and structural roles make up approximately 99% of the human genome, which does not contain proteins. Non-coding RNAs (ncRNA) have been discovered to be essential novel regulators of cardiovascular risk factors and cellular processes, making them significant prospects for advanced diagnostics and prognosis evaluation. Cases of CVDs are rising due to limitations in the current therapeutic approach; most of the treatment options are based on the coding transcripts that encode proteins. Recently, various investigations have shown the role of nc-RNA in the early diagnosis and treatment of CVDs. Furthermore, the development of novel diagnoses and treatments based on miRNAs, lncRNAs, and circRNAs could be more helpful in the clinical management of patients with CVDs. CVDs are classified into various types of heart diseases, including cardiac hypertrophy (CH), heart failure (HF), rheumatic heart disease (RHD), acute coronary syndrome (ACS), myocardial infarction (MI), atherosclerosis (AS), myocardial fibrosis (MF), arrhythmia (ARR), and pulmonary arterial hypertension (PAH). Here, we discuss the biological and clinical importance of miRNAs, lncRNAs, and circRNAs and their expression profiles and manipulation of non-coding transcripts in CVDs, which will deliver an in-depth knowledge of the role of ncRNAs in CVDs for progressing new clinical diagnosis and treatment. Full article

(This article belongs to the Special Issue Non Coding RNA in Cardiovascular Biology and Medicine)

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