Non-coding RNAs in Cardiac Regeneration

Yuan, Ting; Krishnan, Jaya

doi:10.3389/fphys.2021.650566

Cited by 23 publications

(24 citation statements)

References 128 publications

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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%

“…Similarly, hsa - miR-590 and hsa - miR-199a , identified by screening for miRNAs promoting proliferation of neonatal cardiomyocytes ( 31 ), are not exclusively expressed in the cardiac lineage, which may suggest that cardiomyocyte-specific pathways have so far escaped identification. Likewise, several long noncoding RNAs were found to direct cardiomyocyte proliferation and cardiac regeneration, including ECRAR (endogenous cardiac regeneration-associated regulator), CRRL (cardiomyocyte regeneration-related lncRNA), and CAREL (cardiac regeneration-related lncRNA) [reviewed in ( 28 )].…”

Section: Introductionmentioning

confidence: 99%

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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%

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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“…The efficacy of drugs must be titrated against their off-target effects, such as negative impacts on the complement system, toxicity related to the vector, or interference with innate immunity [ 2 , 26 , 27 ]. Although some antago-miRs have been used in clinical trials against the hepatitis C virus and in other conditions [ 28 , 29 , 30 ], no study has investigated their role in cardiac tumors.…”

Section: Future Therapeutic Implicationsmentioning

confidence: 99%

miRNAs in Cardiac Myxoma: New Pathologic Findings for Potential Therapeutic Opportunities

Nenna

Loreni

Giacinto

et al. 2022

IJMS

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MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, contributing to all major cellular processes. The importance of miRNAs in cardiac development, heart function, and valvular heart disease has been shown in recent years, and aberrant expression of miRNA has been reported in various malignancies, such as gastric cancer and breast cancer. Different from other fields of investigation, the role of miRNAs in cardiac tumors still remains difficult to interpret due to the scarcity publications and a lack of narrative focus on this topic. In this article, we summarize the available evidence on miRNAs and cardiac myxomas and propose new pathways for future research. miRNAs play a part in modifying the expression of cardiac transcription factors (miR-335-5p), increasing cell cycle trigger factors (miR-126-3p), interfering with ceramide synthesis (miR-320a), inducing apoptosis (miR-634 and miR-122), suppressing production of interleukins (miR-217), and reducing cell proliferation (miR-218). As such, they have complex and interconnected roles. At present, the study of the complete mechanistic control of miRNA remains a crucial issue, as proper understanding of signaling pathways is essential for the forecasting of therapeutic implications. Other types of cardiac tumors still lack adequate investigation with regard to miRNA. Further research should aim at investigating the causal relationship between different miRNAs and cell overgrowth, considering both myxoma and other histological types of cardiac tumors. We hope that this review will help in understanding this fascinating molecular approach.

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“…Non-coding RNAs (ncRNAs) such as miRNAs, lncRNAs and circular RNAs (circR-NAs), play an important role in the regulation of physiologic and pathologic signaling pathways in cardiomyocytes and can be used to regulate apoptosis in CVDs and improve cardiac tissue regeneration [109]. Yan and colleagues demonstrated that in vitro overexpression of miR-31a-5p, a leading member of the miRNA-31 family, can protect against apoptosis and increase myocardial cell survival through suppression of angiotensin II-induced apoptotic pathway and caspase-3 activity by targeting Tp53 [110].…”

Section: Gene Therapy To Reduce Apoptosismentioning

confidence: 99%

Recent Advances in Gene Therapy for Cardiac Tissue Regeneration

Kim

Zharkinbekov

Sarsenova

et al. 2021

IJMS

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Cardiovascular diseases (CVDs) are responsible for enormous socio-economic impact and the highest mortality globally. The standard of care for CVDs, which includes medications and surgical interventions, in most cases, can delay but not prevent the progression of disease. Gene therapy has been considered as a potential therapy to improve the outcomes of CVDs as it targets the molecular mechanisms implicated in heart failure. Cardiac reprogramming, therapeutic angiogenesis using growth factors, antioxidant, and anti-apoptotic therapies are the modalities of cardiac gene therapy that have led to promising results in preclinical studies. Despite the benefits observed in animal studies, the attempts to translate them to humans have been inconsistent so far. Low concentration of the gene product at the target site, incomplete understanding of the molecular pathways of the disease, selected gene delivery method, difference between animal models and humans among others are probable causes of the inconsistent results in clinics. In this review, we discuss the most recent applications of the aforementioned gene therapy strategies to improve cardiac tissue regeneration in preclinical and clinical studies as well as the challenges associated with them. In addition, we consider ongoing gene therapy clinical trials focused on cardiac regeneration in CVDs.

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Non-coding RNAs in Cardiac Regeneration

Cited by 23 publications

References 128 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

miRNAs in Cardiac Myxoma: New Pathologic Findings for Potential Therapeutic Opportunities

Recent Advances in Gene Therapy for Cardiac Tissue Regeneration

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