Non‐coding RNAs in cardiomyocyte proliferation and cardiac regeneration: Dissecting their therapeutic values

Dong, Xiaoxuan; Xiuyun, Dong; Gao, Feng; Liu, Ning; Liang, Tian; Zhang, Feng; Fu, Xuyang; Pu, Linbin; Chen, Jinghai

doi:10.1111/jcmm.16300

Cited by 9 publications

(6 citation statements)

References 109 publications

(305 reference statements)

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“…To fill this gap, we focused on microRNAs (miRNAs), which potently regulate multiple targets at the posttranscriptional level and modulate various steps during cardiovascular development ( 26 ). Numerous miRNAs have been described to regulate cardiomyocyte proliferation and heart repair [reviewed in ( 27 , 28 )]. Examples include miR-195 ( 29 ) and miR-99/100 ( 30 ), which have been identified to promote expression of cell cycle genes in cardiomyocytes after knockdown or promote cardiomyocyte dedifferentiation and proliferation.…”

Section: Introductionmentioning

confidence: 99%

Repression of Osmr and Fgfr1 by miR-1/133a prevents cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

et al. 2021

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Dedifferentiation of cardiomyocytes is part of the survival program in the remodeling myocardium and may be essential for enabling cardiomyocyte proliferation. In addition to transcriptional processes, non-coding RNAs play important functions for the control of cell cycle regulation in cardiomyocytes and cardiac regeneration. Here, we demonstrate that suppression of FGFR1 and OSMR by miR-1/133a is instrumental to prevent cardiomyocyte dedifferentiation and cell cycle entry in the adult heart. Concomitant inactivation of both miR-1/133a clusters in adult cardiomyocytes activates expression of cell cycle regulators, induces a switch from fatty acid to glycolytic metabolism, and changes expression of extracellular matrix genes. Inhibition of FGFR and OSMR pathways prevents most effects of miR-1/133a inactivation. Short-term miR-1/133a depletion protects cardiomyocytes against ischemia, while extended loss of miR-1/133a causes heart failure. Our results demonstrate a crucial role of miR-1/133a-mediated suppression of Osmr and Ffgfr1 in maintaining the postmitotic differentiated state of cardiomyocytes.

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Section: Introductionmentioning

confidence: 99%

Repression of Osmr and Fgfr1 by miR-1/133a prevents cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

et al. 2021

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“…Second, the interaction of RBPs with non-coding RNAs adds another layer of regulation for repairing the injured heart. Indeed, accumulating evidence suggests that non-coding RNAs also function as important post-transcriptional regulators of CM proliferation and present strong potential as therapeutic targets [108][109][110]. It is of note that RBPs and non-coding RNAs mutually regulate the biogenesis and function of each other, thereby ensuring CM survival and proliferation following cardiac injury.…”

Section: Discussionmentioning

confidence: 99%

RNA-Binding Proteins as Critical Post-Transcriptional Regulators of Cardiac Regeneration

Shi

2023

IJMS

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Myocardial injury causes death to cardiomyocytes and leads to heart failure. The adult mammalian heart has very limited regenerative capacity. However, the heart from early postnatal mammals and from adult lower vertebrates can fully regenerate after apical resection or myocardial infarction. Thus, it is of particular interest to decipher the mechanism underlying cardiac regeneration that preserves heart structure and function. RNA-binding proteins, as key regulators of post-transcriptional gene expression to coordinate cell differentiation and maintain tissue homeostasis, display dynamic expression in fetal and adult hearts. Accumulating evidence has demonstrated their importance for the survival and proliferation of cardiomyocytes following neonatal and postnatal cardiac injury. Functional studies suggest that RNA-binding proteins relay damage-stimulated cell extrinsic or intrinsic signals to regulate heart regenerative capacity by reprogramming multiple molecular and cellular processes, such as global protein synthesis, metabolic changes, hypertrophic growth, and cellular plasticity. Since manipulating the activity of RNA-binding proteins can improve the formation of new cardiomyocytes and extend the window of the cardiac regenerative capacity in mammals, they are potential targets of therapeutic interventions for cardiovascular disease. This review discusses our evolving understanding of RNA-binding proteins in regulating cardiac repair and regeneration, with the aim to identify important open questions that merit further investigations.

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“…For example, the expression of LUCAT1 is aberrant in the tissues of patients with non-small-cell lung cancer or hepatocellular carcinoma [ 27 , 28 ]. Furthermore, LUCAT1 is downregulated in the patients with chronic heart failure, which ptovides an involvement between LUCAT1 and heart disease [ 29 ]. In addition, in a study published in 2020, the authors describe the expression of LINC00528 in cell models of myocardial infarction and explore its roles.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA LUCAT1 inhibits myocardial oxidative stress and apoptosis after myocardial infarction via targeting microRNA-181a-5p

Xiao

Wang²,

Cao

et al. 2021

Bioengineered

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This study hoped to explore the effects and mechanism of long non-coding RNA (lncRNA) LUCAT1 regulating microRNA-181a-5p (miR-181a-5p) on oxidative stress and apoptosis of cardiomyocytes induced by H 2 O 2 . Totally, 72 patients with acute myocardial infarction (AMI) were included. H9c2 cardiomyocytes were cultured in vitro, and the H 2 O 2 model of cardiomyocytes was established. The expression levels of LUCAT1 and miR-181a-5p were detected by qRT-PCR after H 2 O 2 induction. The contents of reactive oxygen species (ROS), superoxide dismutase (SOD), and malondialdehyde (MDA) in cells were detected. The survival rate of the cells was detected by the Cell Counting Kit-8 (CCK-8) method; the apoptosis was detected by flow cytometry. The luciferase reporter experiment and quantitative real-time PCR (qRT-PCR) were used to verify the targeted relationship between LUCAT1 and miR-181a-5p. LUCAT1 was lowly expressed in the AMI patients. After H 2 O 2 induction, the expression of LUCAT1 in H9c2 cells lessened significantly, while the expression of miR-181a-5p elevated significantly ( P < 0.001). Transfection of p-LUCAT1 significantly reversed the decreased SOD levels, the increased MDA and ROS content, and the elevated tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) in H 2 O 2 -stimulated cells ( P < 0.001). Upregulation of LUCAT1 contributed to the mitigation of H 2 O 2 injury by promoting viable cells and repressing apoptotic cells ( P < 0.01). LUCAT1 targeted miR-181a-5p and negatively regulated miR-181a-5p expression ( P < 0.001). Collectively, LUCAT1 played a protective role on oxidative stress injury, inflammation, viability, and apoptosis of cardiomyocytes induced by H 2 O 2 via regulating miR-181a-5p.

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Non‐coding RNAs in cardiomyocyte proliferation and cardiac regeneration: Dissecting their therapeutic values

Cited by 9 publications

References 109 publications

Repression of Osmr and Fgfr1 by miR-1/133a prevents cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

Repression of Osmr and Fgfr1 by miR-1/133a prevents cardiomyocyte dedifferentiation and cell cycle entry in the adult heart

RNA-Binding Proteins as Critical Post-Transcriptional Regulators of Cardiac Regeneration

Long non-coding RNA LUCAT1 inhibits myocardial oxidative stress and apoptosis after myocardial infarction via targeting microRNA-181a-5p

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