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Author

Thomas J. Hawke

Other affiliations: York University, University of Guelph, Keele University  ...read more
Bio: Thomas J. Hawke is an academic researcher from McMaster University. The author has contributed to research in topics: Skeletal muscle & Myocyte. The author has an hindex of 33, co-authored 101 publications receiving 5744 citations. Previous affiliations of Thomas J. Hawke include York University & University of Guelph.


Papers
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TL;DR: This review will highlight the origin and unique markers of the satellite cell population, the regulation by growth factors, and the response to physiological and pathological stimuli, and identify future research goals for the study of satellite cell biology.
Abstract: Adult skeletal muscle has a remarkable ability to regenerate following myotrauma. Because adult myofibers are terminally differentiated, the regeneration of skeletal muscle is largely dependent on a small population of resident cells termed satellite cells. Although this population of cells was identified 40 years ago, little is known regarding the molecular phenotype or regulation of the satellite cell. The use of cell culture techniques and transgenic animal models has improved our understanding of this unique cell population; however, the capacity and potential of these cells remain ill-defined. This review will highlight the origin and unique markers of the satellite cell population, the regulation by growth factors, and the response to physiological and pathological stimuli. We conclude by highlighting the potential therapeutic uses of satellite cells and identifying future research goals for the study of satellite cell biology.

1,647 citations

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TL;DR: The adult heart contains an Abcg2 expressing SP cell population and these progenitor cells are capable of proliferation and differentiation, and it is proposed that the cardiac SPcell population functions as a progenitors cell population for the development, maintenance, and repair of the heart.

678 citations

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TL;DR: It is concluded that muscle regeneration is a complex process that requires the coordinated modulation of the inflammatory response, myogenic progenitor cells, growth factors, and ECM for complete restoration of muscle architecture.
Abstract: Muscle regeneration is a complex process requiring the coordinated interaction between the myogenic progenitor cells or satellite cells, growth factors, cytokines, inflammatory components, vascular components and the extracellular matrix (ECM). Previous studies have elegantly described the physiological modulation of the regenerative process in response to muscle injury, but the molecular response that characterizes stages of the repair process remains ill-defined. The recent completion of the Human and Mouse Genome Projects and the advent of technologies such as high-density oligonucleotide array analysis facilitate an expanded analysis of complex processes such as muscle regeneration. In the present study, we define cellular and molecular events that characterize stages of muscle injury and regeneration. Utilization of transcriptional profiling strategies revealed coordinated expression of growth factors [i.e., Tgfb1, Igf1, Egf, chemokine (C-C motif) ligand 6 and 7], the fetal myogenic program (Myod1, Myf5, Myf6), and the biomatrix (procollagen genes, Mmp3, Mmp9, biglycan, periostin) during muscle regeneration. Corroboration of the transcriptional profiling analysis included quantitative real-time RT-PCR and in situ hybridization analyses of selected candidate genes. In situ hybridization studies for periostin [osteoblast-specific factor 2 (fasciclin I-like)] and biglycan revealed that these genes are restricted to mesenchymal derivatives during embryogenesis and are significantly regulated during regeneration of the injured hindlimb skeletal muscle. We conclude that muscle regeneration is a complex process that requires the coordinated modulation of the inflammatory response, myogenic progenitor cells, growth factors, and ECM for complete restoration of muscle architecture.

263 citations

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TL;DR: Novel evidence is provided that defective adrenergic receptor signaling combined with upregulation of ATGL and suppression of HSL and AMPK signaling mediate HFD-induced alterations in lipolysis and lipid utilization in VC and SC adipocytes, which may play an important role in defective lipid mobilization and metabolism seen in diet-induced obesity.
Abstract: This study investigated the molecular mechanisms by which a high-fat diet (HFD) dysregulates lipolysis and lipid metabolism in mouse epididymal (visceral, VC) and inguinal (subcutaneous, SC) adipoc...

248 citations

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TL;DR: In response to a high-fat diet, iβ1β2AKO mice more rapidly developed liver steatosis as well as glucose and insulin intolerance, and AMPK in adipocytes is vital for maintaining mitochondrial integrity, responding to pharmacological agents and thermal stress, and protecting against nutrient-overload-induced NAFLD and insulin resistance.

243 citations


Cited by
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Journal ArticleDOI
TL;DR: Gaining a better insight into the mechanisms of stem-cell resistance to chemotherapy might lead to new therapeutic targets and better anticancer strategies.
Abstract: The contribution of tumorigenic stem cells to haematopoietic cancers has been established for some time, and cells possessing stem-cell properties have been described in several solid tumours. Although chemotherapy kills most cells in a tumour, it is believed to leave tumour stem cells behind, which might be an important mechanism of resistance. For example, the ATP-binding cassette (ABC) drug transporters have been shown to protect cancer stem cells from chemotherapeutic agents. Gaining a better insight into the mechanisms of stem-cell resistance to chemotherapy might therefore lead to new therapeutic targets and better anticancer strategies.

3,480 citations

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TL;DR: Recent evidence supports the possible contribution of adult stem cells in the muscle regeneration process and in particular, bone marrow-derived and muscle-derived stem cells contribute to new myofiber formation and to the satellite cell pool after injury.
Abstract: Charge, Sophie B. P., and Michael A. Rudnicki. Cellular and Molecular Regulation of Muscle Regeneration. Physiol Rev 84: 209–238, 2004; 10.1152/physrev.00019.2003.—Under normal circumstances, mamma...

2,497 citations

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TL;DR: How AMPK functions as a central mediator of the cellular response to energetic stress and mitochondrial insults and coordinates multiple features of autophagy and mitochondrial biology is discussed.
Abstract: Cells constantly adapt their metabolism to meet their energy needs and respond to nutrient availability. Eukaryotes have evolved a very sophisticated system to sense low cellular ATP levels via the serine/threonine kinase AMP-activated protein kinase (AMPK) complex. Under conditions of low energy, AMPK phosphorylates specific enzymes and growth control nodes to increase ATP generation and decrease ATP consumption. In the past decade, the discovery of numerous new AMPK substrates has led to a more complete understanding of the minimal number of steps required to reprogramme cellular metabolism from anabolism to catabolism. This energy switch controls cell growth and several other cellular processes, including lipid and glucose metabolism and autophagy. Recent studies have revealed that one ancestral function of AMPK is to promote mitochondrial health, and multiple newly discovered targets of AMPK are involved in various aspects of mitochondrial homeostasis, including mitophagy. This Review discusses how AMPK functions as a central mediator of the cellular response to energetic stress and mitochondrial insults and coordinates multiple features of autophagy and mitochondrial biology.

1,873 citations

Journal ArticleDOI
TL;DR: For the last half century, the advance of molecular biology, cell biology, and genetics has greatly improved the understanding of skeletal muscle biology, with focuses on functions of satellite cells and their niche during the process ofletal muscle regeneration.
Abstract: Adult skeletal muscle in mammals is a stable tissue under normal circumstances but has remarkable ability to repair after injury. Skeletal muscle regeneration is a highly orchestrated process invol...

1,585 citations

Journal ArticleDOI
10 Jan 2019-Cell
TL;DR: The biological functions of autophagy genes are discussed from the perspective of understanding-and potentially reversing-the pathophysiology of human disease and aging.

1,432 citations