David A. Hood

Hood attended Fisher Park High School in Ottawa.{{cite web | url=https://dhood.lab.yorku.ca/david-a-hood/ | title=Dr. David A. Hood | Dr. Hood's Laboratory at York University }} Hood received his Bachelor's degree of Physical Education from Queen’s University in 1979 and his Master's degree of Science from Dalhousie University in 1981. He defended his Ph.D. dissertation in Physiology at the State University of New York Health Science Center at Syracuse in 1986.{{cite journal|url=https://pubmed.ncbi.nlm.nih.gov/3425710/|title=Leucine metabolism in perfused rat skeletal muscle during contractions|year=1987|pmid=3425710|last1=Hood|first1=D. A.|last2=Terjung|first2=R. L.|journal=The American Journal of Physiology|volume=253|issue=6 Pt 1|pages=E636-47|doi=10.1152/ajpendo.1987.253.6.E636}} Hood then spent two years as a Post-Doctoral Fellow at the University of Konstanz in Germany.

Following his postdoctoral fellowship, Hood joined York University’s School of Kinesiology and Health Science, and the Department of Biology (Faculty of Graduate Studies) as an assistant professor in 1988. Hood became an associate professor in 1992, and full professor in 1999.

Hood is the founding director, since 2009, of York University’s Muscle Health Research Centre (MHRC).{{Cite web|url=https://mhrc.info.yorku.ca/|title=Muscle Health Research Centre (MHRC)}}

Hood has published over 180 full-paper academic publications in peer-reviewed journals and book chapters as well as greater than 260 abstracts with his trainees. His research program is focused on the study of "Mitochondrial Turnover in Health and Disease”, with a focus on mammalian skeletal muscle and the role of exercise and/or disuse and aging.{{cite journal|url=https://pubmed.ncbi.nlm.nih.gov/30216742/|title=Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging|year=2019|pmid=30216742|last1=Hood|first1=D. A.|last2=Memme|first2=J. M.|last3=Oliveira|first3=A. N.|last4=Triolo|first4=M.|journal=Annual Review of Physiology|volume=81|pages=19–41|doi=10.1146/annurev-physiol-020518-114310|s2cid=52276340 }} He has used a number of in vivo and cell culture experimental models to interrogate the mechanisms of both mitochondrial synthesis (biogenesis), as well as degradation (mitophagy) in muscle. In his research, he also employs multi-disciplinary approaches involving physiological, biochemical and molecular biology techniques.

In 1987, Hood examined leucine metabolism during steady-state conditions as a function of leucine concentration and metabolic rate (VO2), and found out that leucine is metabolized by muscle but is not a major contributor to the energy cost of muscle contractions. His research also indicated that mitochondrial and nuclear gene products are coordinately regulated during adaptations to contractile activity.{{cite journal|title=Chronic stimulation of rat skeletal muscle induces coordinate increases in mitochondrial and nuclear mRNAs of cytochrome-c-oxidase subunits|year=1989|doi=10.1111/j.1432-1033.1989.tb14551.x|last1=Hood|first1=David A.|last2=Zak|first2=Radovan|last3=Pette|first3=Dirk|journal=European Journal of Biochemistry|volume=179|issue=2|pages=275–280|pmid=2537205|doi-access=free}}

In his work, Hood also provided an extensive description of mitochondrial and performance decrements during chronic muscle disuse.{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.00181.2010|title=Effect of denervation-induced muscle disuse on mitochondrial protein import|year=2011|doi=10.1152/ajpcell.00181.2010|last1=Singh|first1=Kaustabh|last2=Hood|first2=David A.|journal=American Journal of Physiology. Cell Physiology|volume=300|issue=1|pages=C138–C145|pmid=20943961|s2cid=2683664 |url-access=subscription}}{{cite journal|url=https://journals.physiology.org/doi/abs/10.1152/ajpcell.1991.260.4.C841|title=Mitochondrial adaptations in denervated muscle: relationship to muscle performance|year=1991|doi=10.1152/ajpcell.1991.260.4.C841|last1=Wicks|first1=K. L.|last2=Hood|first2=D. A.|journal=American Journal of Physiology. Cell Physiology|volume=260|issue=4|pages=C841–C850|pmid=1850197|url-access=subscription}} He was the first to determine that thyroid hormone modifies mitochondria in heart and muscle during growth and development, and repairs mitochondrial defects in diseased cells, in part via increases in protein import.{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.1998.275.6.C1508|title=Thyroid hormone modifies mitochondrial phenotype by increasing protein import without altering degradation|year=1998|doi=10.1152/ajpcell.1998.275.6.C1508|last1=Craig|first1=Elaine E.|last2=Chesley|first2=Alan|last3=Hood|first3=David A.|journal=American Journal of Physiology. Cell Physiology|volume=275|issue=6|pages=C1508–C1515|pmid=9843712|url-access=subscription}}{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.00415.2007|title=Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects|year=2009|doi=10.1152/ajpcell.00415.2007|last1=Menzies|first1=Keir J.|last2=Robinson|first2=Brian H.|last3=Hood|first3=David A.|journal=American Journal of Physiology. Cell Physiology|volume=296|issue=2|pages=C355–C362|pmid=19036942|s2cid=34017256 |url-access=subscription}}{{Cite journal|title=Calcium-dependent Regulation of Cytochromec Gene Expression in Skeletal Muscle Cells: IDENTIFICATION OF A PROTEIN KINASE C-DEPENDENT PATHWAY *|first1=Damien|last1=Freyssenet|first2=Martino Di|last2=Carlo|first3=David A.|last3=Hood|date=April 2, 1999|journal=Journal of Biological Chemistry|volume=274|issue=14|pages=9305–9311|doi=10.1074/jbc.274.14.9305|pmid=10092607|doi-access=free}} He along with co-workers also discovered that contractile activity (i.e. exercise) induces calcium, AMP kinase and reactive oxygen species signaling to increase the transcription of nuclear genes, leading to mitochondrial biogenesis.{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.00418.2003|title=Calcium-regulated changes in mitochondrial phenotype in skeletal muscle cells|year=2004|doi=10.1152/ajpcell.00418.2003|last1=Freyssenet|first1=Damien|last2=Irrcher|first2=Isabella|last3=Connor|first3=Michael K.|last4=Di Carlo|first4=Martino|last5=Hood|first5=David A.|journal=American Journal of Physiology. Cell Physiology|volume=286|issue=5|pages=C1053–C1061|pmid=15075204|s2cid=30135488 |url-access=subscription}} He also conducted a number of studies on muscle mitochondrial biogenesis, and found out that it occurs via the increased expression of fusion, compared to fission regulatory proteins,{{cite journal|url=https://onlinelibrary.wiley.com/doi/abs/10.1002/mus.23838|title=Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse|year=2013|doi=10.1002/mus.23838|last1=Iqbal|first1=Sobia|last2=Ostojic|first2=Olga|last3=Singh|first3=Kaustabh|last4=Joseph|first4=Anna-Maria|last5=Hood|first5=David A.|journal=Muscle & Nerve|volume=48|issue=6|pages=963–970|pmid=23494933|s2cid=31225025|url-access=subscription}} and is accompanied by accelerated protein import into a growing mitochondrial reticulum as a result of exercise.{{Cite journal|title=Protein Import into Subsarcolemmal and Intermyofibrillar Skeletal Muscle Mitochondria: DIFFERENTIAL IMPORT REGULATION IN DISTINCT SUBCELLULAR REGIONS *|first1=Mark|last1=Takahashi|first2=David A.|last2=Hood|date=November 1, 1996|journal=Journal of Biological Chemistry|volume=271|issue=44|pages=27285–27291|doi=10.1074/jbc.271.44.27285|pmid=8910303 |doi-access=free}}{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.1998.274.5.C1380|title=Contractile activity-induced adaptations in the mitochondrial protein import system|year=1998|doi=10.1152/ajpcell.1998.274.5.C1380|last1=Takahashi|first1=Mark|last2=Chesley|first2=Alan|last3=Freyssenet|first3=Damien|last4=Hood|first4=David A.|journal=American Journal of Physiology. Cell Physiology|volume=274|issue=5|pages=C1380–C1387|pmid=9612226|url-access=subscription}}

In a series of papers published in 2007 and 2009, Hood discussed that mitochondrially-mediated cell death (apoptosis) in muscle is increased with age and disuse, and attenuated with exercise.{{cite journal|url=https://onlinelibrary.wiley.com/doi/full/10.1111/j.1474-9726.2007.00347.x|title=Mitochondrial function and apoptotic susceptibility in aging skeletal muscle|year=2008|doi=10.1111/j.1474-9726.2007.00347.x|last1=Chabi|first1=Béatrice|last2=Ljubicic|first2=Vladimir|last3=Menzies|first3=Keir J.|last4=Huang|first4=Julianna H.|last5=Saleem|first5=Ayesha|last6=Hood|first6=David A.|journal=Aging Cell|volume=7|issue=1|pages=2–12|pmid=18028258|s2cid=37302965}}{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpendo.00311.2006|title=Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle|year=2007|doi=10.1152/ajpendo.00311.2006|last1=Adhihetty|first1=Peter J.|last2=Ljubicic|first2=Vladimir|last3=Hood|first3=David A.|journal=American Journal of Physiology. Endocrinology and Metabolism|volume=292|issue=3|pages=E748–E755|pmid=17106065|s2cid=24854658 |url-access=subscription}}{{cite journal|title=Molecular basis for an attenuated mitochondrial adaptive plasticity in aged skeletal muscle|year=2009|pmc=2815739|last1=Ljubicic|first1=V.|last2=Joseph|first2=A. M.|last3=Adhihetty|first3=P. J.|last4=Huang|first4=J. H.|last5=Saleem|first5=A.|last6=Uguccioni|first6=G.|last7=Hood|first7=D. A.|journal=Aging|volume=1|issue=9|pages=818–830|doi=10.18632/aging.100083|pmid=20157569}} He was also the pioneer in providing descriptions of how p53 controls mitochondrial content and function in muscle via exercise, in part via signaling and interaction with mtDNA.{{cite journal|title=Acute exercise induces tumour suppressor protein p53 translocation to the mitochondria and promotes a p53–Tfam–mitochondrial DNA complex in skeletal muscle|year=2013|doi=10.1113/jphysiol.2013.252791|last1=Saleem|first1=Ayesha|last2=Hood|first2=David A.|journal=The Journal of Physiology|volume=591|issue=14|pages=3625–3636|pmid=23690562|pmc=3731618}}{{cite journal|title=p53 is necessary for the adaptive changes in cellular milieu subsequent to an acute bout of endurance exercise|year=2013|pmc=3919998|last1=Saleem|first1=A.|last2=Carter|first2=H. N.|last3=Hood|first3=D. A.|journal=American Journal of Physiology. Cell Physiology|volume=306|issue=3|pages=C241–C249|doi=10.1152/ajpcell.00270.2013|pmid=24284795}} His research further indicated that exercise induces lysosomal biogenesis in skeletal muscle and overcomes lysosomal impairments leading to improved mitochondrial function.{{cite journal|title=Autophagy and mitophagy flux in young and aged skeletal muscle following chronic contractile activity|year=2018|pmc=6092298|last1=Carter|first1=H. N.|last2=Kim|first2=Y.|last3=Erlich|first3=A. T.|last4=Zarrin-Khat|first4=D.|last5=Hood|first5=D. A.|journal=The Journal of Physiology|volume=596|issue=16|pages=3567–3584|doi=10.1113/JP275998|pmid=29781176}}{{cite journal|title= Contractile activity attenuates autophagy suppression and reverses mitochondrial defects in skeletal muscle cells|year= 2018|doi= 10.1080/15548627.2018.1491488|last1= Parousis|first1= Alexa|last2= Carter|first2= Heather N.|last3= Tran|first3= Claudia|last4= Erlich|first4= Avigail T.|last5= Mesbah Moosavi|first5= Zahra S.|last6= Pauly|first6= Marion|last7= Hood|first7= David A.|journal= Autophagy|volume= 14|issue= 11|pages= 1886–1897|pmid= 30078345|pmc= 6152519}} Hood’s research contributed to define the role of mitochondria in terms of sending retrograde signals to the nucleus to activate gene expression in response to mitochondrial stress in muscle.{{cite journal|title=Chronology of UPR activation in skeletal muscle adaptations to chronic contractile activity|year=2016|doi=10.1152/ajpcell.00009.2016|last1=Memme|first1=Jonathan M.|last2=Oliveira|first2=Ashley N.|last3=Hood|first3=David A.|journal=American Journal of Physiology. Cell Physiology|volume=310|issue=11|pages=C1024–C1036|pmid=27122157|pmc=4935206}}{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.00191.2003|title= Compensatory responses of protein import and transcription factor expression in mitochondrial DNA defects|year= 2004|doi= 10.1152/ajpcell.00191.2003|last1= Joseph|first1= Anna-Maria|last2= Rungi|first2= Arne A.|last3= Robinson|first3= Brian H.|last4= Hood|first4= David A.|journal= American Journal of Physiology. Cell Physiology|volume= 286|issue= 4|pages= C867–C875|pmid= 14656719|url-access= subscription}} He also explored the role of PGC-1α and claimed that it is not required to restore mitochondrial respiratory function as a result of exercise,{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpcell.00070.2009|title=The role of PGC-1α on mitochondrial function and apoptotic susceptibility in muscle|year=2009|doi=10.1152/ajpcell.00070.2009|last1=Adhihetty|first1=Peter J.|last2=Uguccioni|first2=Giulia|last3=Leick|first3=Lotte|last4=Hidalgo|first4=Juan|last5=Pilegaard|first5=Henriette|last6=Hood|first6=David A.|journal=American Journal of Physiology. Cell Physiology|volume=297|issue=1|pages=C217–C225|pmid=19439529|url-access=subscription}} but it is required for the normal exercise-induced signaling of nuclear gene expression and the induction of mitophagy.{{cite journal|title= Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle|year= 2015|doi= 10.1152/ajpcell.00380.2014|last1= Vainshtein|first1= Anna|last2= Tryon|first2= Liam D.|last3= Pauly|first3= Marion|last4= Hood|first4= David A.|journal= American Journal of Physiology. Cell Physiology|volume= 308|issue= 9|pages= C710–C719|pmid= 25673772|pmc= 4420796}}

Hood gave the first definition of a role for parkin in exercising and aging skeletal muscle,{{cite journal|title=Parkin is required for exercise-induced mitophagy in muscle: impact of aging|year=2018|doi=10.1152/ajpendo.00391.2017|last1=Chen|first1=Chris Chin Wah|last2=Erlich|first2=Avigail T.|last3=Crilly|first3=Matthew J.|last4=Hood|first4=David A.|journal=American Journal of Physiology. Endocrinology and Metabolism|volume=315|issue=3|pages=E404–E415|pmid=29812989|doi-access=free}} and demonstrated that exercise serves as “Mitochondrial Medicine” for muscle.{{cite journal|url=https://journals.physiology.org/doi/full/10.1152/ajpendo.00043.2007|title=The effect of training on the expression of mitochondrial biogenesis- and apoptosis-related proteins in skeletal muscle of patients with mtDNA defects|year=2007|doi=10.1152/ajpendo.00043.2007|last1=Adhihetty|first1=Peter J.|last2=Taivassalo|first2=Tanja|last3=Haller|first3=Ronald G.|last4=Walkinshaw|first4=Donald R.|last5=Hood|first5=David A.|journal=American Journal of Physiology. Endocrinology and Metabolism|volume=293|issue=3|pages=E672–E680|pmid=17551003|url-access=subscription}}{{cite journal|title= Exercise Is Muscle Mitochondrial Medicine|year= 2021|pmid= 33720909|last1= Oliveira|first1= A. N.|last2= Richards|first2= B. J.|last3= Slavin|first3= M.|last4= Hood|first4= D. A.|journal= Exercise and Sport Sciences Reviews|volume= 49|issue= 2|pages= 67–76|doi= 10.1249/JES.0000000000000250|doi-access= }} Furthermore, he discovered that exercise and resveratrol synergistically increase mitochondria in muscles.{{Cite journal|title=Sirtuin 1-mediated effects of exercise and resveratrol on mitochondrial biogenesis|first1=Keir J.|last1=Menzies|first2=Kaustabh|last2=Singh|first3=Ayesha|last3=Saleem|first4=David A.|last4=Hood|date=March 8, 2013|journal=The Journal of Biological Chemistry|volume=288|issue=10|pages=6968–6979|doi=10.1074/jbc.M112.431155|pmid=23329826|pmc=3591607|doi-access=free }}

Hood and his wife have four children.

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Category:Living people

Category:Queen's University at Kingston alumni

Category:Dalhousie University alumni

Category:State University of New York Upstate Medical University alumni

Category:Academic staff of York University

Category:Exercise physiologists

Category:Year of birth missing (living people)