Recent Advances in the Role of Translation Machinery and Translational Control in the Cardiovascular System

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 4787

Special Issue Editors


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Guest Editor
Department of Biochemistry and Biophysics, Center for RNA Biology, Center for Biomedical Informatics, University of Rochester Medical Center, Rochester, NY, USA
Interests: determine the pathophysiological function and regulatory mechanism of noncoding RNAs (e.g., microRNA and regulatory elements in mRNA untranslated regions); RNA-binding proteins in cardiac system and cardiovascular disorders
Department of Animal and Dairy Sciences, University of Wisconsin, Madison, WI 53706, USA
Interests: muscle structure and function; cardiomyopathies; RNA metabolism; protein trafficking
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Special Issue Information

Dear Colleagues,

Cardiovascular diseases are being recognized at an accelerating frequency and are a cause of heart failure. The major types of cardiovascular diseases include coronary artery disease (CAD), peripheral artery disease (PAD), stroke, and heart diseases such as hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), restrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), genetic cardiomyopathy, and ischemic cardiomyopathy (caused by myocardial infarction). For instance, in cardiomyopathy, the heart muscle becomes enlarged, thick, or rigid, which can lead to other cardiac conditions such as valve problems, blood clots, heart failure, cardiac arrest, and sudden death. The underlying molecular and cellular mechanisms of pathological changes and transition from cardiovascular disease to cardiomyopathy and heart failure remain poorly defined. In addition, congenital defects in vascular and cardiac development can cause cardiovascular disease. The role of translation machinery and the subsequent translational control of protein synthesis is increasingly attracting researchers’ attention in the field of cardiovascular systems and related diseases. Translational regulations occur when ribosomes are loaded to mature mRNAs by translation initiation factors, followed by translation elongation for decoding individual genetic codons to translate mRNA into a protein product. This process includes the translation preinitiation complex binding to the 5’ cap and scanning through the 5’ untranslated region (UTR), ribosome assembly at the start codons to initiate translation, ribosome-directed translation elongation on the coding sequence (CDS), and translation termination at the stop codon, involving translational control by many trans-acting RNA-binding proteins, translation factors, kinases, and signaling molecules. Thus, we invite investigators to contribute original research articles and review articles focused on the role of translation machinery and translational control in physiological homeostasis and pathological changes in the cardiovascular system.

Potential topics include, but are not limited to, the following:

  • Translational control of cardiovascular development and diseases;
  • Function and mechanism of translation factors and RNA-binding proteins in the pathological changes in the cardiovascular system;
  • Role of non-coding RNAs in the regulation of protein synthesis in cardiovascular disease and heart failure;
  • Signaling pathways in translational regulation to the structural and functional alterations of the heart and blood vessels;
  • Novel translation-manipulating therapeutic approaches in cardiovascular disease.

Dr. Peng Yao
Dr. Wei Guo
Guest Editors

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Keywords

  • translational control
  • translation machinery
  • RNA-binding protein
  • non-coding RNA

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Published Papers (3 papers)

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Research

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22 pages, 27687 KiB  
Article
RNA-Binding Protein Signature in Proliferative Cardiomyocytes: A Cross-Species Meta-Analysis from Mouse, Pig, and Human Transcriptomic Profiling Data
by Thanh Nguyen, Kaili Hao, Yuji Nakada, Bijay Guragain, Peng Yao and Jianyi Zhang
Biomolecules 2025, 15(2), 310; https://doi.org/10.3390/biom15020310 - 19 Feb 2025
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Abstract
In mammals, because cardiomyocytes withdraw from cell-cycle activities shortly after birth, the heart cannot repair the damage caused by a myocardial injury; thus, understanding how cardiomyocytes proliferate is among the most important topics in cardiovascular sciences. In newborn neonatal mammals, when a left [...] Read more.
In mammals, because cardiomyocytes withdraw from cell-cycle activities shortly after birth, the heart cannot repair the damage caused by a myocardial injury; thus, understanding how cardiomyocytes proliferate is among the most important topics in cardiovascular sciences. In newborn neonatal mammals, when a left ventricular injury is applied in hearts earlier than postnatal day 7, the cardiomyocytes actively proliferate and regenerate lost myocardium in the following weeks. The regulators promoting cardiomyocyte proliferation were discovered by analyzing transcriptomic data generated from models. Most of these regulators support the mRNA production of cell-cycle machinery, yet the mRNA requires translation into functional proteins under the regulation of RNA-binding proteins (RBPs). In this work, we performed a meta-analysis to study the relationship between RBP expression and cardiomyocyte proliferation. To identify RBPs associated with mouse and pig cardiomyocyte proliferation, the single-nuclei RNA sequencing (snRNA-seq) data from regenerating mouse and pig hearts were reanalyzed via an Autoencoder focusing on RBP expression. We also generated and analyzed new bulk RNA-seq from two human-induced pluripotent stem cell-derived (hiPSC) cardiomyocyte (hiPSC-CM) cell lines; the first cell line was harvested sixteen days after differentiation, when the cells still actively proliferated, and the second cell line was harvested one hundred and forty days after differentiation, when the cells ceased cell cycle activity. Then, the RBP associated with mouse, pig, and hiPSC-CM were compared across species. Twenty-one RBPs were found to be consistently upregulated, and six RBPs were downregulated in proliferating mouse, pig, and hiPSC-derived cardiomyocytes. Among upregulated RBPs across species, an immunofluorescence-based imaging analysis validated the significant increase in the proteins of DHX9, PTBP3, HNRNPUL1, and DDX6 in pig hearts with proliferating CMs. This meta-analysis in all species demonstrated a strong relationship between RBP expression and cardiomyocyte proliferation. Full article
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Review

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15 pages, 5036 KiB  
Review
Exploring the Spectrum of Long Non-Coding RNA CARMN in Physiological and Pathological Contexts
by Hui Li, Chuannan Sun, Bin Luo, Chuzhi Zhan, Weitao Li, Lu Deng, Kang Kang and Deming Gou
Biomolecules 2024, 14(8), 954; https://doi.org/10.3390/biom14080954 - 6 Aug 2024
Cited by 1 | Viewed by 2050
Abstract
Cardiac mesoderm enhancer-associated non-coding RNA (CARMN), an evolutionarily conserved long non-coding RNA (lncRNA), serves as the host gene for the miR143/145 cluster. It plays a crucial role in cardiovascular cell differentiation and the maintenance of vascular smooth muscle cell (VSMC) homeostasis, which are [...] Read more.
Cardiac mesoderm enhancer-associated non-coding RNA (CARMN), an evolutionarily conserved long non-coding RNA (lncRNA), serves as the host gene for the miR143/145 cluster. It plays a crucial role in cardiovascular cell differentiation and the maintenance of vascular smooth muscle cell (VSMC) homeostasis, which are vital for normal physiological processes. Specifically, CARMN is associated with the pathological progression of cardiovascular diseases such as atherosclerosis, abdominal aortic aneurysm, and chronic heart failure. Moreover, it acts as a tumor suppressor in various cancers, including hepatocellular carcinoma, bladder cancer, and breast cancer, highlighting its potential as a beneficial biomarker and therapeutic target. This review provides a detailed examination of the roles of CARMN, its evolutionary conservation, expression patterns, and regulatory mechanisms. It also outlines its significant implications in the diagnosis, prognosis, and treatment of these diseases, underscoring the need for further translational research to exploit its clinical potential. Full article
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Other

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21 pages, 1179 KiB  
Systematic Review
Cytokine Gene Variants as Predisposing Factors for the Development and Progression of Coronary Artery Disease: A Systematic Review
by Fang Li, Yingshuo Zhang, Yichao Wang, Xiaoyan Cai and Xiongwei Fan
Biomolecules 2024, 14(12), 1631; https://doi.org/10.3390/biom14121631 - 19 Dec 2024
Cited by 1 | Viewed by 907
Abstract
Coronary artery disease (CAD) is the most prevalent form of cardiovascular disease. A growing body of research shows that interleukins (ILs), such as IL-8, IL-18 and IL-16, elicit pro-inflammatory responses and may play critical roles in the pathologic process of CAD. Single nucleotide [...] Read more.
Coronary artery disease (CAD) is the most prevalent form of cardiovascular disease. A growing body of research shows that interleukins (ILs), such as IL-8, IL-18 and IL-16, elicit pro-inflammatory responses and may play critical roles in the pathologic process of CAD. Single nucleotide polymorphisms (SNPs), capable of generating functional modifications in IL genes, appear to be associated with CAD risk. This study aims to evaluate the associations of ten previously identified SNPs of the three cytokines with susceptibility to or protection of CAD. A systematic review and meta-analysis were conducted using Pubmed, EMBASE, WOS, CENTRAL, CNKI, CBM, Weipu, WANFANG Data and Google Scholar databases for relevant literature published up to September 2024. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for the four genetic models of the investigated SNPs in overall and subgroups analyses. Thirty-eight articles from 16 countries involving 14574 cases and 13001 controls were included. The present meta-analysis revealed no significant association between CAD and IL-8-rs2227306 or five IL-16 SNPs (rs8034928, rs3848180, rs1131445, rs4778889 and rs11556218). However, IL-8-rs4073 was significantly associated with an increased risk of CAD across all genetic models. In contrast, three IL-18 (rs187238, rs1946518 and rs1946519) variants containing minor alleles were associated with decreased risks of CAD under all models. Subgroups analyses by ethnicity indicated that IL-8-rs4073 conferred a significantly higher risk of CAD among Asians, including East, South and West Asians (allelic OR = 1.46, homozygous OR = 1.96, heterozygous OR = 1.47, dominant OR = 1.65), while it showed an inversely significant association with CAD risk in Caucasians (homozygous OR = 0.82, dominant OR = 0.85). Additionally, IL-18-rs187238 and IL-18-rs1946518 were significantly associated with reduced CAD risks in East Asians (for rs187238: allelic OR = 0.72, homozygous OR = 0.33, heterozygous OR = 0.73, dominant OR = 0.71; for rs1946518: allelic OR = 0.62, homozygous OR = 0.38, heterozygous OR = 0.49, dominant OR = 0.45). IL-18-rs187238 also demonstrated protective effects in Middle Eastern populations (allelic OR = 0.76, homozygous OR = 0.63, heterozygous OR = 0.72, dominant OR = 0.71). No significant associations were observed in South Asians or Caucasians for these IL-18 SNPs. Consistent with the overall analysis results, subgroups analyses further highlighted a significant association between IL-8-rs4073 and increased risk of acute coronary syndrome (heterozygous OR = 0.72). IL-18-rs187238 was significantly associated with decreased risks of myocardial infarction (MI) (allelic OR = 0.81, homozygous OR = 0.55, dominant OR = 0.80) and multiple vessel stenosis (allelic OR = 0.54, heterozygous OR = 0.45, dominant OR = 0.45). Similarly, IL-18-rs1946518 was significantly associated with reduced MI risk (allelic OR = 0.75, heterozygous OR = 0.68). These findings support the role of cytokine gene IL-8 and IL-18 variants as predisposing factors for the development and progression of CAD. Full article
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