Melatonin promotes cardiomyocyte proliferation and heart repair in mice with myocardial infarction via miR-143-3p/Yap/Ctnnd1 signaling pathway

Ma, Wanbiao; Song, Robert X.-D.; Xu, Binbin; Xu, Yan; Wang, Xiuxiu; Sun, Hongyue; Li, Shuai-nan; Liu, Shenzhen; Yu, Meixi; Yang, Fan; Ye, Danyu; Gong, Rui; Han, Zhenbo; Yu, Ying; Bamba, Djibril; Wang, Ning; Pan, Zhenwei; Cai, Benzhi

doi:10.1038/s41401-020-0495-2

Cited by 49 publications

(37 citation statements)

References 41 publications

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“…Melatonin, an amino acid-derived hormone produced by the pineal gland, exerting a protective role against oxidative stress, apoptosis, and inflammation after cardiac injury, has also been documented to induce cardiomyocyte proliferation after myocardial infarction in the mouse model (185). The suggested mechanism involves the activation of the melatonin receptor and regulation of the miR-143-YAP axis (185) (further described in "miRNAs" section).…”

Section: Systemic Hormonesmentioning

confidence: 99%

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Reawakening the Intrinsic Cardiac Regenerative Potential: Molecular Strategies to Boost Dedifferentiation and Proliferation of Endogenous Cardiomyocytes

Bongiovanni

Sacchi

Pra

et al. 2021

Front. Cardiovasc. Med.

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Despite considerable efforts carried out to develop stem/progenitor cell-based technologies aiming at replacing and restoring the cardiac tissue following severe damages, thus far no strategies based on adult stem cell transplantation have been demonstrated to efficiently generate new cardiac muscle cells. Intriguingly, dedifferentiation, and proliferation of pre-existing cardiomyocytes and not stem cell differentiation represent the preponderant cellular mechanism by which lower vertebrates spontaneously regenerate the injured heart. Mammals can also regenerate their heart up to the early neonatal period, even in this case by activating the proliferation of endogenous cardiomyocytes. However, the mammalian cardiac regenerative potential is dramatically reduced soon after birth, when most cardiomyocytes exit from the cell cycle, undergo further maturation, and continue to grow in size. Although a slow rate of cardiomyocyte turnover has also been documented in adult mammals, both in mice and humans, this is not enough to sustain a robust regenerative process. Nevertheless, these remarkable findings opened the door to a branch of novel regenerative approaches aiming at reactivating the endogenous cardiac regenerative potential by triggering a partial dedifferentiation process and cell cycle re-entry in endogenous cardiomyocytes. Several adaptations from intrauterine to extrauterine life starting at birth and continuing in the immediate neonatal period concur to the loss of the mammalian cardiac regenerative ability. A wide range of systemic and microenvironmental factors or cell-intrinsic molecular players proved to regulate cardiomyocyte proliferation and their manipulation has been explored as a therapeutic strategy to boost cardiac function after injuries. We here review the scientific knowledge gained thus far in this novel and flourishing field of research, elucidating the key biological and molecular mechanisms whose modulation may represent a viable approach for regenerating the human damaged myocardium.

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Section: Systemic Hormonesmentioning

confidence: 99%

“…Recently melatonin administration or METTL3 ablation have been shown to downregulate miR-143, in turn enhancing the expression of YAP, thus leading to neonatal cardiomyocyte proliferation (185) and heart regeneration (224).…”

Section: Epigenetic Regulationsmentioning

confidence: 99%

Reawakening the Intrinsic Cardiac Regenerative Potential: Molecular Strategies to Boost Dedifferentiation and Proliferation of Endogenous Cardiomyocytes

Bongiovanni

Sacchi

Pra

et al. 2021

Front. Cardiovasc. Med.

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“…Notably, recent studies have reported the cardioprotective effects of melatonin in various cardiovascular disorders [27][28][29][30][31][32]. For example, preclinical data showed that melatonin alleviates hyperglycemia-mediated cardiomyocyte damage through improving Sirt6-dependent mitochondrial quality control [33] and attenuates myocardial infarction by stimulating cardiomyocyte proliferation via the miRNA-regulated Ctnnd1 pathway [34]. Melatonin was shown to reduce the incidence of myocardial damage in Alzheimer's disease through modulation of cGAS-STING-TBK1-mediated mitophagy [35] and to inhibit abnormal calcium accumulation in aortic valve through the circ-RNA-mediated-DPP4 pathway [36].…”

Section: Introductionmentioning

confidence: 99%

[Retracted] Melatonin Attenuates Cardiac Ischemia‐Reperfusion Injury through Modulation of IP3R‐Mediated Mitochondria‐ER Contact

Liu

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Although the interplay between mitochondria and ER has been identified as a crucial regulator of cellular homeostasis, the pathogenic impact of alterations in mitochondria-ER contact sites (MERCS) during myocardial postischemic reperfusion (I/R) injury remains incompletely understood. Therefore, in our study, we explored the beneficial role played by melatonin in protecting cardiomyocytes against reperfusion injury via stabilizing mitochondria-ER interaction. In vitro exposure of H9C2 rat cardiomyocytes to hypoxia/reoxygenation (H/R) augmented mitochondrial ROS synthesis, suppressed both mitochondrial potential and ATP generation, and increased the mitochondrial permeability transition pore (mPTP) opening rate. Furthermore, H/R exposure upregulated the protein content of CHOP and caspase-12, two markers of ER stress, and enhanced the transcription of main MERCS tethering proteins, namely, Fis1, BAP31, Mfn2, and IP3R. Interestingly, all the above changes could be attenuated or reversed by melatonin treatment. Suggesting that melatonin-induced cardioprotection works through normalization of mitochondria-ER interaction, overexpression of IP3R abolished the protective actions offered by melatonin on mitochondria-ER fitness. These results expand our knowledge on the cardioprotective actions of melatonin during myocardial postischemic reperfusion damage and suggest that novel, more effective treatments for acute myocardial reperfusion injury might be achieved through modulation of mitochondria-ER interaction in cardiac cells.

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“…Up Up [132,136,160,173,200,201] Aggravating Induces apoptosis targeting FABP3, regulates oxidative stress in IRI [162,202] miR-320 Up Up [37,132,135,200] Aggravating Increases infarct size and promotes apoptosis via the inhibition of AKIP1, IGF-1, HSP20, and AKT3 [137][138][139]203]. Aggravating: Promotes cardiac ischemia-mediated mitochondrial impairment by the inhibition of protein kinase C epsilon [250], inhibits the mitosis of cardiomyocytes [251], promotes fibrosis via targeting sprouty3 [252];Attenuating: Promotes post-MI cell proliferation and reduced cell apoptosis in vitro via cyclooxygenase-2 [253] miR-223 Up * Up [136,173,196,[254][255][256]] Ambiguous…”

Section: Mir-192mentioning

confidence: 99%

Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury

Majka

Kleibert

Wojciechowska

2021

Cells

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The majority of cardiovascular deaths are associated with acute coronary syndrome, especially ST-elevation myocardial infarction. Therapeutic reperfusion alone can contribute up to 40 percent of total infarct size following coronary artery occlusion, which is called ischemia-reperfusion injury (IRI). Its size depends on many factors, including the main risk factors of cardiovascular mortality, such as age, sex, systolic blood pressure, smoking, and total cholesterol level as well as obesity, diabetes, and physical effort. Extracellular vesicles (EVs) are membrane-coated particles released by every type of cell, which can carry content that affects the functioning of other tissues. Their role is essential in the communication between healthy and dysfunctional cells. In this article, data on the variability of the content of EVs in patients with the most prevalent cardiovascular risk factors is presented, and their influence on IRI is discussed.

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Melatonin promotes cardiomyocyte proliferation and heart repair in mice with myocardial infarction via miR-143-3p/Yap/Ctnnd1 signaling pathway

Cited by 49 publications

References 41 publications

Reawakening the Intrinsic Cardiac Regenerative Potential: Molecular Strategies to Boost Dedifferentiation and Proliferation of Endogenous Cardiomyocytes

Reawakening the Intrinsic Cardiac Regenerative Potential: Molecular Strategies to Boost Dedifferentiation and Proliferation of Endogenous Cardiomyocytes

[Retracted] Melatonin Attenuates Cardiac Ischemia‐Reperfusion Injury through Modulation of IP3R‐Mediated Mitochondria‐ER Contact

Impact of the Main Cardiovascular Risk Factors on Plasma Extracellular Vesicles and Their Influence on the Heart’s Vulnerability to Ischemia-Reperfusion Injury

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