Mechanisms of Neonatal Heart Regeneration

Cardoso, Alisson C.; Pereira, Ana Helena Macedo; Sadek, Hesham A.

doi:10.1007/s11886-020-01282-5

Cited by 26 publications

(28 citation statements)

References 110 publications

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“…Understanding variations in the repair process (i.e. the robust regeneration seen in some fish and amphibians compared with the ineffective repair observed in birds and mammal species) has been a topic of intense investigation for many years (Oberpriller and Oberpriller, 1974;Flink, 2002;Hsieh et al, 2007;Laflamme and Murry, 2011;Tzahor and Poss, 2017;Cardoso et al, 2020) (Fig. 2).…”

Section: The Role Of Cncc-derived Cardiomyocytes In Cardiac Regenerationmentioning

confidence: 99%

“…The major impediment to murine cardiac regeneration appears to be the inability of cardiomyocytes to become proliferative (Pasumarthi and Field, 2002). Gaining an understanding of the molecular mechanisms driving cardiomyocyte cell cycle re-entry has been rigorously researched for the last two decades, with multiple pathways implicated in this process (Cardoso et al, 2020). To date however, based on results generated from current cell lineage tracing tools, it still remains unclear whether mouse cNCCs can adopt a cardiomyocyte lineage, let alone whether preexisting cNCC-derived cardiomyocytes can contribute to efficacious heart regeneration.…”

Section: The Role Of Cncc-derived Cardiomyocytes In Cardiac Regenerationmentioning

confidence: 99%

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The heart of the neural crest: cardiac neural crest cells in development and regeneration

2020

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Cardiac neural crest cells (cNCCs) are a migratory cell population that stem from the cranial portion of the neural tube. They undergo epithelial-to-mesenchymal transition and migrate through the developing embryo to give rise to portions of the outflow tract, the valves and the arteries of the heart. Recent lineage-tracing experiments in chick and zebrafish embryos have shown that cNCCs can also give rise to mature cardiomyocytes. These cNCC-derived cardiomyocytes appear to be required for the successful repair and regeneration of injured zebrafish hearts. In addition, recent work examining the response to cardiac injury in the mammalian heart has suggested that cNCC-derived cardiomyocytes are involved in the repair/regeneration mechanism. However, the molecular signature of the adult cardiomyocytes involved in this repair is unclear. In this Review, we examine the origin, migration and fates of cNCCs. We also review the contribution of cNCCs to mature cardiomyocytes in fish, chick and mice, as well as their role in the regeneration of the adult heart.

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Section: The Role Of Cncc-derived Cardiomyocytes In Cardiac Regenerationmentioning

confidence: 99%

Section: The Role Of Cncc-derived Cardiomyocytes In Cardiac Regenerationmentioning

confidence: 99%

The heart of the neural crest: cardiac neural crest cells in development and regeneration

2020

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“…It also appears possible to reprogram resident cardiac fibroblasts to adopt a CM fate by using small molecule inhibitors of transforming growth factor beta and WNT, which resulted in successful transdifferentiation and improved ventricular function in mice ( Mohamed et al, 2017 ). Interestingly, zebrafish retain regenerative capacity throughout their life and have a relatively hypoxic circulatory system as a result of veno-arterial mixing in their two-chamber heart, similar to the shunt dependent phase of mammalian gestation ( Cardoso et al, 2020 ). This hypoxic environment drives anaerobic glycolysis, the predominant energy source in the prenatal heart.…”

Section: Natural Regenerationmentioning

confidence: 99%

Navigating the Crossroads of Cell Therapy and Natural Heart Regeneration

Elde

Wang

Woo

2021

Front. Cell Dev. Biol.

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Cardiovascular disease remains the leading cause of death worldwide despite significant advances in our understanding of the disease and its treatment. Consequently, the therapeutic potential of cell therapy and induction of natural myocardial regeneration have stimulated a recent surge of research and clinical trials aimed at addressing this challenge. Recent developments in the field have shed new light on the intricate relationship between inflammation and natural regeneration, an intersection that warrants further investigation.

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“…In contrast, cardiomyocytes and non-cardiomyocyte populations in invertebrates regenerate after myocardial damage. The current paradigm is that mammals' hearts are able to regenerate during the prenatal period, and exposure to atmospheric oxygen in the days after birth causes their heart muscle cells to stop proliferating [17]. However, there is a transition period from a hypoxic intrauterine environment to the postnatal environment with ambient air oxygen.…”

Section: Myocardial Regenerationmentioning

confidence: 99%

Targeting myocardial ischaemic injury in the absence of reperfusion

Basalay¹,

Yellon²,

Davidson³

2020

Basic Res Cardiol

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Sudden myocardial ischaemia causes an acute coronary syndrome. In the case of ST-elevation myocardial infarction (STEMI), this is usually caused by the acute rupture of atherosclerotic plaque and obstruction of a coronary artery. Timely restoration of blood flow can reduce infarct size, but ischaemic regions of myocardium remain in up to two-thirds of patients due to microvascular obstruction (MVO). Experimentally, cardioprotective strategies can limit infarct size, but these are primarily intended to target reperfusion injury. Here, we address the question of whether it is possible to specifically prevent ischaemic injury, for example in models of chronic coronary artery occlusion. Two main types of intervention are identified: those that preserve ATP levels by reducing myocardial oxygen consumption, (e.g. hypothermia; cardiac unloading; a reduction in heart rate or contractility; or ischaemic preconditioning), and those that increase myocardial oxygen/blood supply (e.g. collateral vessel dilation). An important consideration in these studies is the method used to assess infarct size, which is not straightforward in the absence of reperfusion. After several hours, most of the ischaemic area is likely to become infarcted, unless it is supplied by pre-formed collateral vessels. Therefore, therapies that stimulate the formation of new collaterals can potentially limit injury during subsequent exposure to ischaemia. After a prolonged period of ischaemia, the heart undergoes a remodelling process. Interventions, such as those targeting inflammation, may prevent adverse remodelling. Finally, harnessing of the endogenous process of myocardial regeneration has the potential to restore cardiomyocytes lost during infarction.

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Mechanisms of Neonatal Heart Regeneration

Cited by 26 publications

References 110 publications

The heart of the neural crest: cardiac neural crest cells in development and regeneration

The heart of the neural crest: cardiac neural crest cells in development and regeneration

Navigating the Crossroads of Cell Therapy and Natural Heart Regeneration

Targeting myocardial ischaemic injury in the absence of reperfusion

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