MiR-1180 promotes cardiomyocyte cell cycle re-entry after injury through the NKIRAS2–NFκB pathway

Ding, Yuhui; Bi, Liyuan; Wang, Jun

doi:10.1139/bcb-2019-0364

Cited by 7 publications

(3 citation statements)

References 35 publications

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“…Ding et al investigated the miR-1180 mechanism on cardiomyocytes and found that the miR-1180 observed in the rat's heart at embryonal day 9.5 decreased over time and completely disappeared at the seven postnatal days ( 34 ). In H/R-induced cardiomyocytes, miR-1180 expression was downregulated.…”

Section: Characterization Of Cardiomyocyte Proliferationmentioning

confidence: 99%

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

Qin

Xie

Tang

et al. 2022

Front. Cardiovasc. Med.

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Cardiovascular diseases remain the leading cause of death worldwide, particularly ischemic heart disease (IHD). It is also classified as incurable given the irreversible damage it causes to cardiomyocytes. Thus, myocardial tissue rejuvenation following ischemia is one of the global primary research concerns for scientists. Interestingly, the mammalian heart thrives after an injury during the embryonic or neonatal period; however, this ability disappears with increasing age. Previous studies have found that specific non-coding (nc) RNAs play a pivotal role in this process. Hence, the review herein summarizes the research on cardiomyocyte regenerative medicine in recent years and sets forth the biological functions and mechanisms of the micro (mi)RNA, long non-coding (lnc)RNA, and circular (circ)RNA in the posttranscriptional regulation of cardiomyocytes. In addition, this review summarizes the roles of ncRNAs in specific species while enumerating potential therapeutic strategies for myocardial infarction.

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Section: Characterization Of Cardiomyocyte Proliferationmentioning

confidence: 99%

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

Qin

Xie

Tang

et al. 2022

Front. Cardiovasc. Med.

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“…PTEN/PI3K/AKT is another signal transduction pathway that is activated by miR-301a to promote cardiomyocyte re-entry into the cell cycle; miR-301a suppresses PTEN to activate AKT and induce expression of cell cycle genes such as cyclin D1, in cardiac myocytes [50]. Other miRNAs have been reported to promote cell cycle progression in cardiomyocytes by targeting the TBX1/JAK2/STAT1 pathway [74], the NFkB pathway [75], or signaling molecules such as the cell cycle inhibitors Wee1 [76] and Bim [77], among others [78,79]. These studies suggest that MiRNAs possess the potential for replenishing cardiomyocyte numbers in injured hearts.…”

Section: Selective Induction/inhibition Of Gene Expression Can Induce Cell Cycle Re-activation In Cardiac Myocytesmentioning

confidence: 99%

Cardiomyocyte Proliferation as a Source of New Myocyte Development in the Adult Heart

Johnson

Mohsin

Houser

2021

IJMS

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Cardiac diseases such as myocardial infarction (MI) can lead to adverse remodeling and impaired contractility of the heart due to widespread cardiomyocyte death in the damaged area. Current therapies focus on improving heart contractility and minimizing fibrosis with modest cardiac regeneration, but MI patients can still progress to heart failure (HF). There is a dire need for clinical therapies that can replace the lost myocardium, specifically by the induction of new myocyte formation from pre-existing cardiomyocytes. Many studies have shown terminally differentiated myocytes can re-enter the cell cycle and divide through manipulations of the cardiomyocyte cell cycle, signaling pathways, endogenous genes, and environmental factors. However, these approaches result in minimal myocyte renewal or cardiomegaly due to hyperactivation of cardiomyocyte proliferation. Finding the optimal treatment that will replenish cardiomyocyte numbers without causing tumorigenesis is a major challenge in the field. Another controversy is the inability to clearly define cardiomyocyte division versus myocyte DNA synthesis due to limited methods. In this review, we discuss several studies that induced cardiomyocyte cell cycle re-entry after cardiac injury, highlight whether cardiomyocytes completed cytokinesis, and address both limitations and methodological advances made to identify new myocyte formation.

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“…However, the Nodal sig ing pathway, an important signal transduction pathway active during embryonic h development [40], is suppressed by miR-33a-5p which targets nodal modulat (NOMO1) [41]. 92, miR-19a/b or miR-221-3p [33][34][35] or silenced by miR-208a and miR-489, which b phosphoinositide 3-kinase (PI3K) and spindlin-1 (SPIN1), respectively [36 Conversely, other pathways appear to be regulated only by pro-proliferative or apoptotic miRNAs, such as the NF-kB pathway which can be activated by blockade of suppressor of cytokine signaling 3 (SOCS3) and the NF-kB inhibitor interacting Ras-li (NKIRAS2) by miR-324 [38] and miR-1180 [39], respectively. However, the Nodal sig ing pathway, an important signal transduction pathway active during embryonic h development [40], is suppressed by miR-33a-5p which targets nodal modulato (NOMO1) [41].…”

Section: Introductionmentioning

confidence: 99%

miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach

Salvatori,

D’Aversa,

Serino

et al. 2023

IJMS

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Myocardial infarction (MI) is one of the leading causes of death in Western countries. An early diagnosis decreases subsequent severe complications such as wall remodeling or heart failure and improves treatments and interventions. Novel therapeutic targets have been recognized and, together with the development of direct and indirect epidrugs, the role of non-coding RNAs (ncRNAs) yields great expectancy. ncRNAs are a group of RNAs not translated into a product and, among them, microRNAs (miRNAs) are the most investigated subgroup since they are involved in several pathological processes related to MI and post-MI phases such as inflammation, apoptosis, angiogenesis, and fibrosis. These processes and pathways are finely tuned by miRNAs via complex mechanisms. We are at the beginning of the investigation and the main paths are still underexplored. In this review, we provide a comprehensive discussion of the recent findings on epigenetic changes involved in the first phases after MI as well as on the role of the several miRNAs. We focused on miRNAs function and on their relationship with key molecules and cells involved in healing processes after an ischemic accident, while also giving insight into the discrepancy between males and females in the prognosis of cardiovascular diseases.

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MiR-1180 promotes cardiomyocyte cell cycle re-entry after injury through the NKIRAS2–NFκB pathway

Cited by 7 publications

References 35 publications

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

Non-coding RNAs to regulate cardiomyocyte proliferation: A new trend in therapeutic cardiac regeneration

Cardiomyocyte Proliferation as a Source of New Myocyte Development in the Adult Heart

miRNAs Epigenetic Tuning of Wall Remodeling in the Early Phase after Myocardial Infarction: A Novel Epidrug Approach

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