Joe Quadrilatero


Cross-Appointed with the Department of Biology, Faculty of Science

Joe Quadrilatero

Contact information

Office: BMH 1106

Phone: 519-888-4567, ext. 48131


Website: Skeletal Muscle Biology and Cell Death Laboratory

Remote video URL

Research interests

The primary focus of the Skeletal Muscle Biology and Cell Death Laboratory is to study cell death processes (i.e., apoptosis and autophagy) in skeletal muscle. In addition, a major theme is the influence of mitochondrial signaling and dynamics on skeletal muscle development, function, regeneration, and health. 

The specific areas of focus of the Skeletal Muscle Biology and Cell Death Laboratory currently are:

Autophagic and Mitophagic Signaling in Skeletal Muscle

Autophagy is a cellular degradation mechanism that aids in the removal of cytoplasmic contents such as macromolecules and organelles, thereby influencing cell survival. It is now well established that dysregulation of apoptotic and autophagic signaling play major roles in tissue dysfunction and in the pathogenesis of numerous diseases. The Skeletal Muscle Biology and Cell Death Laboratory is at the forefront of understand the role of autophagy and mitophagy (a specialized form of mitochondrial autophagy) in the formation and maintenance of skeletal muscle. We recently discovered that autophagy is required for skeletal muscle differentiation.

Apoptotic Signaling in Skeletal Muscle

Apoptosis is a highly conserved cell death mechanism that allows multi-cellular organisms to maintain tissue and cellular homeostasis. The Skeletal Muscle Biology and Cell Death Laboratory is defining some of the important differences in apoptotic signaling and susceptibility between muscles, fiber types, and mitochondria. We are also investigating the critical role of oxidative stress and mitochondrial content/function on apoptotic susceptibility, and defining key apoptotic signaling aspects that are essential in skeletal muscle differentiation and formation.

Interplay between Autophagy and Apoptosis during Cell Death and Myogenesis

The Skeletal Muscle Biology and Cell Death Laboratory is investigating the interplay between autophagic and apoptotic signaling in skeletal muscle. Recently, our lab discovered that autophagy regulates caspase activation and degrades damaged and dysfunctional mitochondria (mitophagy) thereby protecting skeletal muscle cells from cell death and allowing for optimal muscle formation.

Role of Mitochondrial Dynamics on Skeletal Muscle Regeneration and Myogenesis

Along with mitophagy, mitochondrial biogenesis is important in mitochondrial dynamics by increasing overall mitochondrial content and mass. In addition, mitochondrial fission and fusion regulate the specific nature of the mitochondrial network. The Skeletal Muscle Biology and Cell Death Laboratory has found that induction of mitochondrial biogenesis and regulation of mitochondrial fission and fusion are critical in proper skeletal muscle formation by influencing apoptotic and autophagic signaling.

Effect of Physical Activity and Diet on Apoptotic and Autophagic Signaling

It is well known that exercise and diet are important in the management and prevention of numerous diseases. Exercise and nutrition influence a number of intracellular signaling pathways. Work from the Skeletal Muscle Biology and Cell Death Laboratory has found that exercise and models that mimic exercise signaling in vitro can alter apoptosis and autophagy in skeletal muscle. New work from our lab is demonstrating the benefits of acute nutritional interventions on skeletal muscle autophagic signaling during skeletal muscle damage and regeneration.

Graduate supervision and student opportunities

  • Research volunteer
  • Undergraduate thesis
  • MSc thesis
  • PhD thesis
  • Postdoctoral fellowship

Please email me to discuss current available opportunities.

Graduate studies application details

Teaching, expertise, tools and technologies

  • Skeletal muscle biology
  • Skeletal muscle disease
  • Exercise physiology
  • Mitochondria
  • Cell and molecular biology
  • Microscopy
  • Cell culture
  • Animal models
  • Cellular imaging


KIN 406: Physiology of Skeletal Muscle Aging & Disease

KIN 606: Molecular Basis of Disease 


PhD, University of Waterloo

​Selected publications

See Google Scholar, PubMed, and Loop for a complete list of publications.

Bloemberg, D. and Quadrilatero J. Autophagy displays divergent roles during intermittent amino acid starvation and toxic stress-induced senescence in cultured skeletal muscle cells. Journal of Cellular Physiology. 2020 doi: 10.1002/jcp.30079.

Bloemberg, D. and Quadrilatero J. Autophagy, apoptosis, and mitochondria: Molecular integration and physiological relevance in skeletal muscle. American Journal of Physiology – Cell Physiology, 2019, 317: C111-C130.

Baechler, B.L., Bloemberg, D., Quadrilatero, J. Mitophagy regulates mitochondrial network signaling, oxidative stress, and apoptosis during myoblast differentiation. Autophagy, 2019, 7: 1-14.

Boonstra, K., Bloemberg, D., Quadrilatero, J. Caspase-2 is required for skeletal muscle differentiation and myogenesis. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2018, 1865: 95-104.

Vorobej, K., Mitchell, A.S., Smith, I.C., Donath, S., Tupling A.R., Quadrilatero, J. The effect of ARC ablation on skeletal muscle morphology, function, and apoptotic signaling during aging. Experimental Gerontology 2018, 101: 69-79.

Paré, M-F., Baechler, B.L., Fajardo, V.A., Earl, E., Wong, E., Campbell, T.L., Tupling, A.R., Quadrilatero, J. Effect of acute and chronic autophagy deficiency on skeletal muscle apoptotic signaling, morphology, and function. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2017, 1864: 708-718.

McMillan, E.M., Paré, M-F., Baechler B.L., Graham, D.A., Rush, J.W.E., Quadrilatero, J. Autophagic signaling and proteolytic enzyme activity in cardiac and skeletal muscle of spontaneously hypertensive rats following chronic aerobic exercise. PLoS ONE, 2015, 10: e0119382. 

Mitchell, A.S., Smith, I.C., Gamu, D., Donath, S., Tupling, A.R., Quadrilatero, J. Functional, morphological, and apoptotic alterations in skeletal muscle of ARC deficient Mice. Apoptosis, 2015, 20: 310-326.