Role of Blood Oxygen Saturation During Post-Natal Human Cardiomyocyte Cell Cycle Activities

Ye, Lincai; Qiu, Lisheng; Feng, Bei; Jiang, Chuan; Huang, Yanhui; Zhang, Haibo; Zhang, Hao; Hong, Haifa; Liu, Jinfen

doi:10.1016/j.jacbts.2020.02.008

Cited by 25 publications

(22 citation statements)

References 40 publications

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“…Following MI, hypoxia treatment improved cardiomyocyte renewal, decreased fibrotic area, and increased cardiac function [51]. Similar results have been seen in cardiac tissue specimens from postnatal human patients with tetralogy of Fallot, where moderate hypoxia reduced oxidative DNA damage and increased cardiomyocyte proliferation [88]. These studies suggest that hypoxia induced preexisting cardiomyocytes to re-enter the cell cycle and divide by altering the mitochondrial metabolism (Figure 2).…”

Section: Changes In Cardiac Myocyte Metabolism Can Induce Cell Cycle Re-entrysupporting

confidence: 67%

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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Section: Changes In Cardiac Myocyte Metabolism Can Induce Cell Cycle Re-entrysupporting

confidence: 67%

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

Johnson

Mohsin

Houser

2021

IJMS

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“…One-week exposure to hypoxemia could induce robust myocardial regeneration from preexisting cardiomyocytes with decreased myocardial fibrosis and improved systolic function in response to myocardial infarction (Nakada et al, 2017). Similar beneficial effects of hypoxia on cardiomyocyte cell cycle activation are also observed in human myocardial tissue and iPSC-derived cardiomyocytes (iPSC-CMs), highlighting that hypoxia could serve as a potential therapeutic path forward toward human myocardial regeneration (Sadek and Olson, 2020;Ye et al, 2020).…”

Section: Regulation Of Cell Cycle Withdrawal In Postnatal Cardiomyocytesmentioning

confidence: 91%

“…NICD/RBPJ activation stimulates BMP10 activity in the underlying myocardium which triggers the proliferation of cardiomyocytes through the inhibition of the cell cycle inhibitor p57 (Grego-Bessa et al, 2007). Notch1 deletion in mouse embryos leads to reduced cardiomyocyte differentiation and impaired ventricular trabeculation, whereas exogenous Bmp10 expression can rescue the phenotype in Notch1 -Bessa et al, 2007;Campa et al, 2008;Chen et al, 2013;Collesi et al, 2008;Luxan et al, 2013 Embryonic proliferation NOTCH Zebrafish Zhao et al, 2014Zhao et al, , 2019a Embryonic proliferation Hippo Mouse Heallen et al, 2011Heallen et al, , 2013Xin et al, 2011Xin et al, , 2013von Gise et al, 2012 Embryonic proliferation iPSC-CM proliferation WNT Human/Mouse Klaus et al, 2012;Buikema et al, 2013Buikema et al, , 2020Wang et al, 2016;Fan et al, 2018 Embryonic proliferation Neuregulin-ERBB Mouse Gassmann et al, 1995;Lee et al, 1995;Meyer and Birchmeier, 1995;Erickson et al, 1997;Bersell et al, 2009;D'Uva et al, 2015 Soonpaa et al, 1997;Engel et al, 2005;Pasumarthi et al, 2005;Sdek et al, 2011;Mahmoud et al, 2013;Nguyen et al, 2020 Postnatal cell cycle exit Hypoxia Mouse Puente et al, 2014;Guimaraes-Camboa et al, 2015;Kimura et al, 2015;Tao et al, 2016;Nakada et al, 2017 Postnatal cell cycle exit Hypoxia Human Ye et al, 2020 Physiological hypertrophy Thyroid hormone Mouse…”

Section: Notch Signaling Pathwaymentioning

confidence: 99%

Cardiomyocyte Proliferation and Maturation: Two Sides of the Same Coin for Heart Regeneration

Zhao

et al. 2020

Front. Cell Dev. Biol.

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In the past few decades, cardiac regeneration has been the central target for restoring the injured heart. In mammals, cardiomyocytes are terminally differentiated and rarely divide during adulthood. Embryonic and fetal cardiomyocytes undergo robust proliferation to form mature heart chambers in order to accommodate the increased workload of a systemic circulation. In contrast, postnatal cardiomyocytes stop dividing and initiate hypertrophic growth by increasing the size of the cardiomyocyte when exposed to increased workload. Extracellular and intracellular signaling pathways control embryonic cardiomyocyte proliferation and postnatal cardiac hypertrophy. Harnessing these pathways could be the future focus for stimulating endogenous cardiac regeneration in response to various pathological stressors. Meanwhile, patient-specific cardiomyocytes derived from autologous induced pluripotent stem cells (iPSCs) could become the major exogenous sources for replenishing the damaged myocardium. Human iPSC-derived cardiomyocytes (iPSC-CMs) are relatively immature and have the potential to increase the population of cells that advance to physiological hypertrophy in the presence of extracellular stimuli. In this review, we discuss how cardiac proliferation and maturation are regulated during embryonic development and postnatal growth, and explore how patient iPSC-CMs could serve as the future seed cells for cardiac cell replacement therapy.

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“…The big question is whether hypoxia can drive cell cycle activity in the human heart. Recently, Ye and colleagues conducted an elegant study showing increased cell cycle activity CMs from human heart samples isolated from patients with cyanotic heart diseases [6]. Authors collected 30 ventricular outflow myocardial tissue specimens from Tetralogy of Fallot patients and categorized them as mild hypoxia, moderate hypoxia and severe hypoxia based on blood oxygen saturation.…”

Section: Oxygen Tensionmentioning

confidence: 99%

Aging in reverse: Reactivating developmental signaling for cardiomyocyte proliferation

Rigaud

Khan

2021

Journal of Molecular and Cellular Cardiology

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Role of Blood Oxygen Saturation During Post-Natal Human Cardiomyocyte Cell Cycle Activities

Cited by 25 publications

References 40 publications

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

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

Cardiomyocyte Proliferation and Maturation: Two Sides of the Same Coin for Heart Regeneration

Aging in reverse: Reactivating developmental signaling for cardiomyocyte proliferation

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