ORCID Profile
0000-0002-2733-3361
Current Organisation
King's College London
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Publisher: Elsevier BV
Date: 04-2007
Publisher: BMJ
Date: 2016
DOI: 10.1136/BJSPORTS-2014-306596REP
Abstract: Cardiorespiratory fitness is a strong predictor of cardiovascular (CV) disease and all-cause mortality, with increases in cardiorespiratory fitness associated with corresponding decreases in CV disease risk. The effects of exercise upon the myocardium and vascular system are dependent upon the frequency, intensity and duration of the exercise itself. Following a prolonged period (≥6 months) of regular intensive exercise in previously untrained in iduals, resting and submaximal exercising heart rates are typically 5-20 beats lower, with an increase in stroke volume of ∼20% and enhanced myocardial contractility. Structurally, all four heart chambers increase in volume with mild increases in wall thickness, resulting in greater cardiac mass due to increased myocardial cell size. With this in mind, the present paper aims to review the basic science behind the CV benefits of exercise. Attention will be paid to understanding (1) the relationship between exercise and cardiac remodelling (2) the cardiac cellular and molecular adaptations in response to exercise, including the examination of molecular mechanisms of physiological cardiac growth and applying these mechanisms to identify new therapeutic targets to prevent or reverse pathological remodelling and heart failure and (3) vascular adaptations in response to exercise. Finally, this review will briefly examine how to optimise the CV benefits of exercise by considering how much and how intense exercise should be.
Publisher: Wiley
Date: 10-03-2019
DOI: 10.1111/ACEL.12931
Publisher: Elsevier BV
Date: 12-2017
Publisher: Springer Science and Business Media LLC
Date: 04-07-2017
Publisher: Oxford University Press (OUP)
Date: 17-04-2014
Abstract: Developing effective strategies for the regeneration of solid tissue requires an understanding of the biology underlying the tissue's endogenous repair mechanisms. PW1/Peg3pos/Pax7neg skeletal muscle-derived interstitial progenitor cells (PICs) were first identified recently in the interstitium of murine skeletal muscle and shown to contribute to muscle fiber regeneration in vivo. PICs, therefore, represent a novel candidate resident progenitor cell for muscle regeneration. To explore the potential of these cells for clinical translation, we must ascertain the presence of PICs in larger mammalian species and identify criteria to successfully isolate and expand this population. In this study, we report the isolation, characterization, and maintenance of multipotent PICs from juvenile porcine skeletal muscle. We show that porcine PICs can be reproducibly isolated from skeletal muscle, express stem rogenitor cell markers, and have a stable phenotype and karyotype through multiple passages. Furthermore, porcine PICs are clonogenic and multipotent, giving rise to skeletal myoblast/myotubes, smooth muscle, and endothelial cells. In addition, PICs can be induced to differentiate into cardiomyocyte-like cells. These results demonstrate, in an animal model with size and physiology extrapolatable to the human, that porcine skeletal muscle-derived PW1pos/Pax7neg PICs are a source of stem rogenitor cells. These findings open new avenues for a variety of solid tissue engineering and regeneration using a single multipotent stem cell type isolated from an easily accessible source, such as skeletal muscle.
Publisher: Elsevier BV
Date: 08-2013
DOI: 10.1016/J.CELL.2013.07.039
Abstract: The epidemic of heart failure has stimulated interest in understanding cardiac regeneration. Evidence has been reported supporting regeneration via transplantation of multiple cell types, as well as replication of postmitotic cardiomyocytes. In addition, the adult myocardium harbors endogenous c-kit(pos) cardiac stem cells (eCSCs), whose relevance for regeneration is controversial. Here, using different rodent models of diffuse myocardial damage causing acute heart failure, we show that eCSCs restore cardiac function by regenerating lost cardiomyocytes. Ablation of the eCSC abolishes regeneration and functional recovery. The regenerative process is completely restored by replacing the ablated eCSCs with the progeny of one eCSC. eCSCs recovered from the host and recloned retain their regenerative potential in vivo and in vitro. After regeneration, selective suicide of these exogenous CSCs and their progeny abolishes regeneration, severely impairing ventricular performance. These data show that c-kit(pos) eCSCs are necessary and sufficient for the regeneration and repair of myocardial damage.
Publisher: Public Library of Science (PLoS)
Date: 26-07-2013
Publisher: BMJ
Date: 24-04-2015
DOI: 10.1136/HEARTJNL-2014-306596
Abstract: Cardiorespiratory fitness is a strong predictor of cardiovascular (CV) disease and all-cause mortality, with increases in cardiorespiratory fitness associated with corresponding decreases in CV disease risk. The effects of exercise upon the myocardium and vascular system are dependent upon the frequency, intensity and duration of the exercise itself. Following a prolonged period (≥6 months) of regular intensive exercise in previously untrained in iduals, resting and submaximal exercising heart rates are typically 5-20 beats lower, with an increase in stroke volume of ∼20% and enhanced myocardial contractility. Structurally, all four heart chambers increase in volume with mild increases in wall thickness, resulting in greater cardiac mass due to increased myocardial cell size. With this in mind, the present paper aims to review the basic science behind the CV benefits of exercise. Attention will be paid to understanding (1) the relationship between exercise and cardiac remodelling (2) the cardiac cellular and molecular adaptations in response to exercise, including the examination of molecular mechanisms of physiological cardiac growth and applying these mechanisms to identify new therapeutic targets to prevent or reverse pathological remodelling and heart failure and (3) vascular adaptations in response to exercise. Finally, this review will briefly examine how to optimise the CV benefits of exercise by considering how much and how intense exercise should be.
Publisher: Wiley
Date: 02-2015
DOI: 10.14814/PHY2.12302
Publisher: Oxford University Press (OUP)
Date: 25-11-2015
DOI: 10.1136/POSTGRADMEDJ-2014-306596REP
Abstract: Cardiorespiratory fitness is a strong predictor of cardiovascular (CV) disease and all-cause mortality, with increases in cardiorespiratory fitness associated with corresponding decreases in CV disease risk. The effects of exercise upon the myocardium and vascular system are dependent upon the frequency, intensity and duration of the exercise itself. Following a prolonged period (≥6 months) of regular intensive exercise in previously untrained in iduals, resting and submaximal exercising heart rates are typically 5–20 beats lower, with an increase in stroke volume of ∼20% and enhanced myocardial contractility. Structurally, all four heart chambers increase in volume with mild increases in wall thickness, resulting in greater cardiac mass due to increased myocardial cell size. With this in mind, the present paper aims to review the basic science behind the CV benefits of exercise. Attention will be paid to understanding (1) the relationship between exercise and cardiac remodelling (2) the cardiac cellular and molecular adaptations in response to exercise, including the examination of molecular mechanisms of physiological cardiac growth and applying these mechanisms to identify new therapeutic targets to prevent or reverse pathological remodelling and heart failure and (3) vascular adaptations in response to exercise. Finally, this review will briefly examine how to optimise the CV benefits of exercise by considering how much and how intense exercise should be.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Georgina Ellison.