Davi Mázala, Ph.D.

Assistant Professor

Davi Mázala

Contact Info

Burdick Hall, 121 T
M/W/F 2-3pm


Ph.D., Kinesiology, University of Maryland, 2016

M.A., Kinesiology, University of Maryland, 2011

B.S., Kinesiology, University of Maryland, 2009

Areas of Expertise

Exercise Physiology
Muscle Physiology
Skeletal Muscle Biology (Regeneration and Myogenesis)
Neuromuscular Diseases
Intracellular Pathways

Davi was initially exposed to research during his first year of college in Brazil, in which he participated in lab activities focused on measuring submaximal VO2 in highly trained runners.  In 2007, he transferred to the Department of Kinesiology at the University of Maryland (UMD), where he performed lab rotations to experience different areas of research (biomechanics, cognitive motor neuroscience, and exercise physiology) within the Kinesiology major.  He decided to join the exercise physiology research group, and study cellular and molecular alterations in muscle diseases, including Duchenne muscular dystrophy (DMD) and Lou Gehrig’s disease (ALS).  While at UMD, his research focused on understanding the mechanisms contributing to different diseases and how exercise training and dietary changes could help ameliorate those symptoms.  In 2016, he joined the Center for Genetic Medicine Research at Children’s National Health System as a NIH T32 post-doctoral fellow. Since joining Children’s, his research focused on evaluating satellite cell function as well as the role of the satellite cell niche on skeletal muscle regeneration (regenerative myogenesis) in different mouse models of DMD.  His exposure to different areas of research as well as different models (humans and animals) has given him a broad view of the research spectrum – from studying whole body responses to exercise training to studying cell and molecular alterations in neuromuscular diseases.  While his education and training has been broad, his primary research goal has always stayed the same: to use his knowledge about cellular, molecular, and whole-body physiology to improve people’s lives.

His exposure to teaching started as early as his second year of college where he served as a teaching assistant (TA) for Exercise Physiology.  During his Masters education, he was also a TA for Exercise Physiology, amongst other activity courses in the Kinesiology major.  Since then, he has always been eager to continue educating and mentoring students, not only on the particular class subject, but also on their future academic and professional endeavors. He continued to contribute to teaching by being associated with the Department of Kinesiology at UMD as an adjunct faculty in the Spring of 2017 and 2020, where he taught an upper level undergraduate course (KNES497 - “Adaptations of Skeletal Muscle with Disease and Exercise Training”).

Select Publications and Presentations

  • Novak J, Mázala DAG, Nearing M, Hindupur R, Habib N, Dickson T, Ioffe OB, Harris BT, Fidelia-Lambert MN, Rossi CT, Hill DA, Wagner KR, Hoffman EP & Partridge T. Human muscle stem cells are refractory to aging. Aging Cell (accepted for publication).  Co-authorship: authors should be regarded as joint first authors and have contributed equally to this work. 

  • Chandra G, Mázala DAG & Jaiswal J. Coping with the calcium overload caused by cell injury: ER to the rescue. Cell Stress(2021); 5(5), 73. 

  • Chandra G, Sreetama SC, Mázala DAG, Charton K, VanderMeulen JH, Richard I & Jaiswal J. Endoplasmic reticulum maintains ion homeostasis required for plasma membrane repair. Journal of Cell Biology (2021); 220 (5).  

  • Mázala DAG, Novak JS, Hogarth MW, Nearing M, Adusumalli P, Tully CB, Habib N, Gordish-Dressman H, Chen Y, Jaiswal J & Partridge TA. TGF-β–driven muscle degeneration and failed regeneration underlie disease onset in a DMD mouse model. Journal of Clinical Investigation Insight (2020); 5(6)
  • Debattisti V, Horn A, Singh R, Seifert EL, Hogarth M, Mázala DAG, Huang KT, Horvath R, Jaiswal J & Hajnóczky G. Dysregulation of mitochondrial Ca2+ uptake and sarcolemma repair underlie muscle weakness and wasting in patients and mice lacking MICU1. Cell Reports (2019); 29(5), 1274-1286
  • Ryu D, Zhang H, Ropelle ER, Sorrentino V, Mázala DAG, Mouchiroud L, Marshall PL, Campbell MD, Ali AS, Knowels GM, Bellemin S, Iyer SR, Wang X, Gariani K, Sauve AA, Cantó C, Conley KE, Walter L, Lovering RM, Chin ER, Jasmin BJ, Marcine DJ, Menzies KJ & Auwerx J. NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation. Science translational medicine 8.361 (2016): 361ra139-361ra139

  • Davidson ZE, Rodden G, Mázala DAG, Moore C, Papillon C, Hasemann AJ, Truby H & Grange RW. Practical Nutrition Guidelines for Individuals with Duchenne Muscular Dystrophy. In Regenerative Medicine for Degenerative Muscle Diseases (pp. 225-279). Springer New York. 2016
  • Mázala DAG, Pratt SJ, Chen D, Molkentin JD, Lovering R & Chin ER. SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models. American Journal of Physiology - Cell Physiology (2015); 308: C699–C709

  • Chin ER, Chen D, Bobyk KD & Mázala DAG. Perturbations in intracellular Ca2+ handling in skeletal muscle of a mouse model of Amyotrophic Lateral Sclerosis. American Journal of Physiology - Cell Physiology (2014); 307: C1031–C1038

Full list of publications:


Courses Taught

  • KNES 265
  • KNES 469