David A. Hood

Research Focus

Our research involves the study of the biogenesis, turnover and function of the mitochondrion in mammalian skeletal muscle. Mitochondria have important roles in determining 1) the energy supply, 2) cell signaling, 3) innate immunity, 4) reactive oxygen species (ROS) production, and 2) the degree of apoptosis in cells. We actively investigate the role of exercise, aging and chronic muscle disuse on mitochondrial function and turnover. A number of experimental models in humans, animals and cells are used to manipulate the rate and extent of mitochondrial biogenesis. In skeletal muscle this includes chronic and acute electrical stimulation in vivo and in cell culture. Physiological, biochemical, and molecular biology techniques are employed using healthy tissues, and tissues obtained from patients with mitochondrial diseases. We focus on the regulation of gene transcription, the signals that activate transcription brought about by exercise, and the post-translational import and assembly of proteins into the newly synthesized organelle. We also study the mechanisms involved in mitochondrial degradation, termed mitophagy, in health, disease and aging muscle, focusing on the involvement of exercise in improving the aging-related decline in muscle function. Current studies also examine the function of the lysosome in mediating mitochondrial disposal when the organelle becomes dysfunctional. This information will help us understand the regulation of mitochondrial turnover in muscle in response to exercise, and it has clinical relevance with respect to understanding the molecular basis of mitochondrial diseases in muscle and other tissues.

Representative Publications

Oliveira A.N., Y. Tamura, J.M. Memme, and D.A. Hood. Role of TFEB and TFE3 in mediating lysosomal and mitochondrial adaptations to contractile activity in muscle cells. Autophagy Reports (in revision, 2023). 

Oliveira A.N., J.M. Memme, J. Wong and D.A. Hood. Dimorphic effect of TFE3 in determining mitochondrial and lysosomal content in muscle following denervation. J. Cachexia, Sarcopenia Muscle (in revision, 2023). 

Memme J.M., V.C. Sanfrancesco, and D.A. Hood. ATF4 regulates mitochondrial content, morphology, and function in skeletal muscle cells. Am. J. Physiol. Cell Physiol. (in revision, 2023). 

Picca A., M. Triolo, S.E. Wohlgemuth, M.S. Martenson, R.T.  Mankowski, S.D. Anton, E Marzetti, C.  Leeuwenburgh, and D.A. Hood. Relationship between Mitochondrial Quality Control Markers, Lower Extremity Tissue Composition, and Physical Performance in Physically Inactive Older Adults. Cells. Jan 2;12(1):183. doi: 10.3390/cells12010183. 2023.

Vainshtein A., M.B. Slavin, A.J. Cheng, J.M. Memme, A.N. Oliveira, C.G.R. Perry, A.A. Abdul-Sater, A.N. Belcastro, M.C. Riddell, M. Triolo, T.L. Haas, E. Roudier, and D.A. Hood. Scientific meeting report: International Biochemistry of Exercise 2022. J Appl Physiol (1985). 133:1381-1393. doi: 10.1152/japplphysiol.00475.2022.

Slavin M.B., R. Kumari, and D.A. Hood. ATF5 is a regulator of exercise-induced mitochondrial quality control in skeletal muscle. Mol Metab. Dec;66:101623. doi: 10.1016/j.molmet.2022.101623, 2022.

Triolo, M. D. Bhattacharya and D. A. Hood. Denervation induces mitochondrial decline but exacerbates lysosome dysfunction in middle-aged mice. Aging. (in press, 2022).

Triolo, M., A.N. Oliveira, R. Kumari and D.A. Hood. The influence of age, sex and exercise on autophagy, mitophagy and lysosome biogenesis in skeletal muscle. Skelet. Muscle 12(1):13. doi: 10.1186/s13395-022-00296-7, 2022.

Slavin, M.B., J.M. Memme, A.N. Oliveira, N. Moradi and D.A. Hood. Regulatory networks coordinating mitochondrial quality control in skeletal muscle. Am J Physiol Cell Physiol. 322: C913-C926. doi: 10.1152/ajpcell.00065.2022.

Triolo, M, M. Slavin, N. Moradi and D.A. Hood. Time-dependent changes in autophagy, mitophagy and lysosomes in skeletal muscle during denervation-induced disuse. J. Physiol. doi: 10.1113/JP282173, 2022.

Memme, J.M., A.N. Oliveira and D. A. Hood.  The importance of TP53/p53 in regulating the mitophagy-lysosomal machinery in muscle following disuse. Autophagy Rep. 1: 75-78, 2022.

Richards, B.J., M. Slavin, A.N. Oliveira, V.C. Sanfrancesco and D.A. Hood.  Mitochondrial protein import and UPR^mt in skeletal muscle remodeling and adaptation. Semin. Cell Develop. Biol. doi.org/10.1016/j.semcdb.2022.01.002, 2022.

Memme, J.M., A.N. Oliveira and D. A. Hood.  p53 regulates skeletal muscle mitophagy and mitochondrial quality control following denervation-induced muscle disuse. J. Biol. Chem. 298: 101540-101558, 2022.

Oliveira, A.N., B. Richards and D.A. Hood. Measurement of protein import capacity of skeletal muscle mitochondria. J Vis Exp. 179. doi: 10.3791/63055, 2022.

Triolo, M. and D.A. Hood. Manifestations of age on autophagy, mitophagy and lysosomes in skeletal muscle. Cells 10(5):1054. doi: 10.3390/cells10051054, 2021.

Memme, J.M, M. Slavin, N. Moradi and D.A. Hood. Mitochondrial Bioenergetics and Turnover During Chronic Muscle Disuse. Int’l. J. Mol. Sci. 22(10):5179. doi: 10.3390/ijms22105179, 2021.

Bonafiglia J.T., H. Islam, N. Preobrazenski, A. Ma, M. Deschenes, A.T. Erlich, J. Quadrilatero, D. A. Hood and B.J. Gurd. Examining interindividual differences in select muscle and whole-body adaptations to continuous endurance training.  Exp Physiol. doi: 10.1113/EP089421,2021.

Picca, A., S.K. Saini, R.T. Mankowski, G. Kamenov, S.D. Anton, T.M. Manini, T.W. Buford, S.E. Wohlgemuth, R. Xiao, R. Calvani, H.J. Coelho-Junior, F. Landi, R. Bernabei, D.A. Hood, E. Marzetti and C. Leeuwenburgh. Altered expression of mitoferrin and frataxin, larger labile iron pool and greater mitochondrial DNA damage in skeletal muscle of older adults. Cells. 9:2579. doi: 10.3390/cells 9122579, 2021.

Oliveira, A.N., B. Yanagawa, S. Verma and D.A. Hood.  Blunted stress response with age in right atrial tissue following ischemia-reperfusion. J. Card Surg. doi: 10.1111/jocs.15807, 2021.

Cheema, N., J.M. Cameron and D.A. Hood.  Mitochondrial dysfunction in fibroblasts with mtDNA defects is attenuated with rapamycin treatment. Am. J. Physiol. Cell Physiol. 321:C176-C186, 2021.

Oliveira, A.N., B. Richards, M. Slavin and D.A. Hood.  Exercise is mitochondrial medicine for muscle. Exerc. Sport Sci. Reviews 49:67-76, 2021.

Memme, J.M. and D.A. Hood. Molecular basis for the therapeutic effects of exercise on mitochondrial defects. Frontiers Physiol.  11:615038. doi: 10.3389/fphys.2020.6150382021, 2021.

Islam, H., D.A Hood and B.J. Gurd. Looking beyond PGC-1α: emerging regulators of exercise-induced skeletal muscle mitochondrial biogenesis and their activation by dietary compounds. Appl Physiol Nutr Metab. 45:11-23, 2020.

Zhang Y, A.N. Oliveira, D.A. Hood. The intersection of exercise and aging on mitochondrial protein quality control. Exp Gerontol.131:110824. doi:10.1016/j.exger.2019.110824, 2020.

Kirkland, A., B.T. Gearity, D. A. Hood et al. Comment on CrossTalk43: Exercise training intensity is/is not more important than volume to promote increases in human skeletal muscle mitochondrial content. J. Physiol, 597: 4111-4113, 2019.

Erlich, A. T. and D. A. Hood. Mitophagy regulation in skeletal muscle: Effect of endurance exercise and age. Journal of Science in Sport and Exercise. 10.1007/s42978-019-00041-5, 2019 

Oliveira, A. N. and D. A. Hood. Exercise is mitochondrial medicine for muscle. Sports Medicine and Health Science. 10.1016/j.smhs.2019.

Memme, J. M., A. T Erlich, G. Phukan, and D. A. Hood. Exercise and mitochondrial health.  J. Physiol. doi:10.1113/JP278853, 2019.

Triolo, M. and D. A. Hood Mitochondrial breakdown in skeletal muscle and the emerging role of lysosomes. Arch. Biochem. Biophys. 661:66-73, 2019.

Kim, Y., M. Triolo, A. T Erlich, and D. A. Hood. Regulation of autophagic and mitophagic flux during chronic contractile activity-induced muscle adaptations. Pfluger’s Arch. 471:431-440, 2019.

Hood, D.A., J.M. Memme, A.N. Oliveira and M. Triolo. Maintenance of skeletal muscle mitochondria in health, exercise, and aging. Ann. Rev. Physiol. 81:19-41, 2019.

Sub-Disciplines

Muscle physiology

Research Areas

UN Goals