David A. Hood

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David A. Hood
Born
Montreal, Canada
NationalityCanadian
Occupation(s)Exercise physiologist, academic and researcher
AwardsHonour Award, Canadian Society of Exercise Physiology (CSEP)
Academic background
EducationQueen's University (BPhEd)
Dalhousie University(MS)
State University of New York Health Science Center at Syracuse(PhD)
Academic work
InstitutionsYork University

David A. Hood is a Canadian professor, exercise physiologist, and Director of the Muscle Health Research Centre at York University. A holder of an NSERC Tier I Canada Research Chair in Cell Physiology,[1] Hood is credited with making significant research advances in understanding of the biology of exercise, mitochondria and muscle health.[2]

Education[edit]

Hood attended Fisher Park High School in Ottawa.[3] 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.[4] Hood then spent two years as a Post-Doctoral Fellow at the University of Konstanz in Germany.[5]

Career[edit]

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.[1]

Hood is the founding director, since 2009, of York University’s Muscle Health Research Centre (MHRC).[6]

Research[edit]

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.[7] 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.[2]

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.[4] His research also indicated that mitochondrial and nuclear gene products are coordinately regulated during adaptations to contractile activity.[5]

In his work, Hood also provided an extensive description of mitochondrial and performance decrements during chronic muscle disuse.[8][9] 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.[10][11][12] 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.[13] 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,[14] and is accompanied by accelerated protein import into a growing mitochondrial reticulum as a result of exercise.[15][16]

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.[17][18][19] 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.[20][21] His research further indicated that exercise induces lysosomal biogenesis in skeletal muscle and overcomes lysosomal impairments leading to improved mitochondrial function.[22][23] 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.[24][25] 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,[26] but it is required for the normal exercise-induced signaling of nuclear gene expression and the induction of mitophagy.[27]

Hood gave the first definition of a role for parkin in exercising and aging skeletal muscle,[28] and demonstrated that exercise serves as “Mitochondrial Medicine” for muscle.[29][30] Furthermore, he discovered that exercise and resveratrol synergistically increase mitochondria in muscles.[31]

Personal life[edit]

Hood and his wife have four children.[3]

References[edit]

  1. ^ a b "Faculty of Health". health.yorku.ca.
  2. ^ a b "David A. Hood". scholar.google.ca.
  3. ^ a b "Dr. David A. Hood | Dr. Hood's Laboratory at York University".
  4. ^ a b Hood, D. A.; Terjung, R. L. (1987). "Leucine metabolism in perfused rat skeletal muscle during contractions". The American Journal of Physiology. 253 (6 Pt 1): E636-47. doi:10.1152/ajpendo.1987.253.6.E636. PMID 3425710.
  5. ^ a b Hood, David A.; Zak, Radovan; Pette, Dirk (1989). "Chronic stimulation of rat skeletal muscle induces coordinate increases in mitochondrial and nuclear mRNAs of cytochrome-c-oxidase subunits". European Journal of Biochemistry. 179 (2): 275–280. doi:10.1111/j.1432-1033.1989.tb14551.x. PMID 2537205.
  6. ^ "Muscle Health Research Centre (MHRC)".
  7. ^ Hood, D. A.; Memme, J. M.; Oliveira, A. N.; Triolo, M. (2019). "Maintenance of Skeletal Muscle Mitochondria in Health, Exercise, and Aging". Annual Review of Physiology. 81: 19–41. doi:10.1146/annurev-physiol-020518-114310. PMID 30216742. S2CID 52276340.
  8. ^ Singh, Kaustabh; Hood, David A. (2011). "Effect of denervation-induced muscle disuse on mitochondrial protein import". American Journal of Physiology. Cell Physiology. 300 (1): C138–C145. doi:10.1152/ajpcell.00181.2010. PMID 20943961. S2CID 2683664.
  9. ^ Wicks, K. L.; Hood, D. A. (1991). "Mitochondrial adaptations in denervated muscle: relationship to muscle performance". American Journal of Physiology. Cell Physiology. 260 (4): C841–C850. doi:10.1152/ajpcell.1991.260.4.C841. PMID 1850197.
  10. ^ Craig, Elaine E.; Chesley, Alan; Hood, David A. (1998). "Thyroid hormone modifies mitochondrial phenotype by increasing protein import without altering degradation". American Journal of Physiology. Cell Physiology. 275 (6): C1508–C1515. doi:10.1152/ajpcell.1998.275.6.C1508. PMID 9843712.
  11. ^ Menzies, Keir J.; Robinson, Brian H.; Hood, David A. (2009). "Effect of thyroid hormone on mitochondrial properties and oxidative stress in cells from patients with mtDNA defects". American Journal of Physiology. Cell Physiology. 296 (2): C355–C362. doi:10.1152/ajpcell.00415.2007. PMID 19036942. S2CID 34017256.
  12. ^ Freyssenet, Damien; Carlo, Martino Di; Hood, David A. (April 2, 1999). "Calcium-dependent Regulation of Cytochromec Gene Expression in Skeletal Muscle Cells: IDENTIFICATION OF A PROTEIN KINASE C-DEPENDENT PATHWAY *". Journal of Biological Chemistry. 274 (14): 9305–9311. doi:10.1074/jbc.274.14.9305. PMID 10092607 – via www.jbc.org.
  13. ^ Freyssenet, Damien; Irrcher, Isabella; Connor, Michael K.; Di Carlo, Martino; Hood, David A. (2004). "Calcium-regulated changes in mitochondrial phenotype in skeletal muscle cells". American Journal of Physiology. Cell Physiology. 286 (5): C1053–C1061. doi:10.1152/ajpcell.00418.2003. PMID 15075204. S2CID 30135488.
  14. ^ Iqbal, Sobia; Ostojic, Olga; Singh, Kaustabh; Joseph, Anna-Maria; Hood, David A. (2013). "Expression of mitochondrial fission and fusion regulatory proteins in skeletal muscle during chronic use and disuse". Muscle & Nerve. 48 (6): 963–970. doi:10.1002/mus.23838. PMID 23494933. S2CID 31225025.
  15. ^ Takahashi, Mark; Hood, David A. (November 1, 1996). "Protein Import into Subsarcolemmal and Intermyofibrillar Skeletal Muscle Mitochondria: DIFFERENTIAL IMPORT REGULATION IN DISTINCT SUBCELLULAR REGIONS *". Journal of Biological Chemistry. 271 (44): 27285–27291. doi:10.1074/jbc.271.44.27285. PMID 8910303 – via www.jbc.org.
  16. ^ Takahashi, Mark; Chesley, Alan; Freyssenet, Damien; Hood, David A. (1998). "Contractile activity-induced adaptations in the mitochondrial protein import system". American Journal of Physiology. Cell Physiology. 274 (5): C1380–C1387. doi:10.1152/ajpcell.1998.274.5.C1380. PMID 9612226.
  17. ^ Chabi, Béatrice; Ljubicic, Vladimir; Menzies, Keir J.; Huang, Julianna H.; Saleem, Ayesha; Hood, David A. (2008). "Mitochondrial function and apoptotic susceptibility in aging skeletal muscle". Aging Cell. 7 (1): 2–12. doi:10.1111/j.1474-9726.2007.00347.x. PMID 18028258. S2CID 37302965.
  18. ^ Adhihetty, Peter J.; Ljubicic, Vladimir; Hood, David A. (2007). "Effect of chronic contractile activity on SS and IMF mitochondrial apoptotic susceptibility in skeletal muscle". American Journal of Physiology. Endocrinology and Metabolism. 292 (3): E748–E755. doi:10.1152/ajpendo.00311.2006. PMID 17106065. S2CID 24854658.
  19. ^ Ljubicic, V.; Joseph, A. M.; Adhihetty, P. J.; Huang, J. H.; Saleem, A.; Uguccioni, G.; Hood, D. A. (2009). "Molecular basis for an attenuated mitochondrial adaptive plasticity in aged skeletal muscle". Aging. 1 (9): 818–830. doi:10.18632/aging.100083. PMC 2815739. PMID 20157569.
  20. ^ Saleem, Ayesha; Hood, David A. (2013). "Acute exercise induces tumour suppressor protein p53 translocation to the mitochondria and promotes a p53–Tfam–mitochondrial DNA complex in skeletal muscle". The Journal of Physiology. 591 (14): 3625–3636. doi:10.1113/jphysiol.2013.252791. PMC 3731618. PMID 23690562.
  21. ^ Saleem, A.; Carter, H. N.; Hood, D. A. (2013). "p53 is necessary for the adaptive changes in cellular milieu subsequent to an acute bout of endurance exercise". American Journal of Physiology. Cell Physiology. 306 (3): C241–C249. doi:10.1152/ajpcell.00270.2013. PMC 3919998. PMID 24284795.
  22. ^ Carter, H. N.; Kim, Y.; Erlich, A. T.; Zarrin-Khat, D.; Hood, D. A. (2018). "Autophagy and mitophagy flux in young and aged skeletal muscle following chronic contractile activity". The Journal of Physiology. 596 (16): 3567–3584. doi:10.1113/JP275998. PMC 6092298. PMID 29781176.
  23. ^ Parousis, Alexa; Carter, Heather N.; Tran, Claudia; Erlich, Avigail T.; Mesbah Moosavi, Zahra S.; Pauly, Marion; Hood, David A. (2018). "Contractile activity attenuates autophagy suppression and reverses mitochondrial defects in skeletal muscle cells". Autophagy. 14 (11): 1886–1897. doi:10.1080/15548627.2018.1491488. PMC 6152519. PMID 30078345.
  24. ^ Memme, Jonathan M.; Oliveira, Ashley N.; Hood, David A. (2016). "Chronology of UPR activation in skeletal muscle adaptations to chronic contractile activity". American Journal of Physiology. Cell Physiology. 310 (11): C1024–C1036. doi:10.1152/ajpcell.00009.2016. PMC 4935206. PMID 27122157.
  25. ^ Joseph, Anna-Maria; Rungi, Arne A.; Robinson, Brian H.; Hood, David A. (2004). "Compensatory responses of protein import and transcription factor expression in mitochondrial DNA defects". American Journal of Physiology. Cell Physiology. 286 (4): C867–C875. doi:10.1152/ajpcell.00191.2003. PMID 14656719.
  26. ^ Adhihetty, Peter J.; Uguccioni, Giulia; Leick, Lotte; Hidalgo, Juan; Pilegaard, Henriette; Hood, David A. (2009). "The role of PGC-1α on mitochondrial function and apoptotic susceptibility in muscle". American Journal of Physiology. Cell Physiology. 297 (1): C217–C225. doi:10.1152/ajpcell.00070.2009. PMID 19439529.
  27. ^ Vainshtein, Anna; Tryon, Liam D.; Pauly, Marion; Hood, David A. (2015). "Role of PGC-1α during acute exercise-induced autophagy and mitophagy in skeletal muscle". American Journal of Physiology. Cell Physiology. 308 (9): C710–C719. doi:10.1152/ajpcell.00380.2014. PMC 4420796. PMID 25673772.
  28. ^ Chen, Chris Chin Wah; Erlich, Avigail T.; Crilly, Matthew J.; Hood, David A. (2018). "Parkin is required for exercise-induced mitophagy in muscle: impact of aging". American Journal of Physiology. Endocrinology and Metabolism. 315 (3): E404–E415. doi:10.1152/ajpendo.00391.2017. PMID 29812989.
  29. ^ Adhihetty, Peter J.; Taivassalo, Tanja; Haller, Ronald G.; Walkinshaw, Donald R.; Hood, David A. (2007). "The effect of training on the expression of mitochondrial biogenesis- and apoptosis-related proteins in skeletal muscle of patients with mtDNA defects". American Journal of Physiology. Endocrinology and Metabolism. 293 (3): E672–E680. doi:10.1152/ajpendo.00043.2007. PMID 17551003.
  30. ^ Oliveira, A. N.; Richards, B. J.; Slavin, M.; Hood, D. A. (2021). "Exercise Is Muscle Mitochondrial Medicine". Exercise and Sport Sciences Reviews. 49 (2): 67–76. doi:10.1249/JES.0000000000000250. PMID 33720909.
  31. ^ Menzies, Keir J.; Singh, Kaustabh; Saleem, Ayesha; Hood, David A. (March 8, 2013). "Sirtuin 1-mediated effects of exercise and resveratrol on mitochondrial biogenesis". The Journal of Biological Chemistry. 288 (10): 6968–6979. doi:10.1074/jbc.M112.431155. PMC 3591607. PMID 23329826.
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