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The primary focus of the Skeletal Muscle Biology & 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 & 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 & 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 & 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 & 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 & 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 & 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.
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
The primary focus of the Skeletal Muscle Biology & 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 & 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 & 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 & 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 & 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 & 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 & 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.
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
研究兴趣
论文共 146 篇作者统计合作学者相似作者
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Irina Bukhteeva, Fasih A. Rahman,Brian Kendall,Robin E. Duncan,Joe Quadrilatero,Evgeny V. Pavlov,Michel J. P. Gingras,Zoya Leonenko
SPINE JOURNALno. 1 (2024): 161-171
Irina Bukhteeva, Fasih A. Rahman,Brian Kendall,Robin E. Duncan,Joe Quadrilatero,Evgeny V. Pavlov,Michel J. P. Gingras,Zoya Leonenko
FRONTIERS IN PHYSIOLOGY (2024)
Irina Bukhteeva, Irina Bukhteeva, Fasih A. Rahman,Brian Kendall,Robin E. Duncan,Joe Quadrilatero,Evgeny V. Pavlov,Michel J. P. Gingras,Michel J. P. Gingras,Zoya Leonenko,Zoya Leonenko,Zoya Leonenko
Journal of the Mechanical Behavior of Biomedical Materials (2024): 106334-106334
Fatemeh Bakhshandeh,Hanjia Zheng,Nicole G Barra, Sadegh Sadeghzadeh,Irfani Ausri,Payel Sen,Fatemeh Keyvani, Fasih Rahman,Joe Quadrilatero,Juewen Liu,Jonathan D Schertzer,Leyla Soleymani,
Advanced materials (Deerfield Beach, Fla.)pp.e2313743-e2313743, (2024)
Irina Bukhteeva, Fasih A Rahman,Brian Kendall,Robin E Duncan,Joe Quadrilatero,Evgeny V Pavlov,Michel J P Gingras,Zoya Leonenko
Frontiers in physiology (2024): 1354091-1354091
Fasih A. Rahman, Dylan J. Hian-Cheong, Kristen Boonstra,Andrew Ma, James P. Thoms, Anderson S. Zago,Joe Quadrilatero
JOURNAL OF CELLULAR PHYSIOLOGY (2024)
Erfan Shirzadi, Michelle Huynh,Peyman GhavamiNejad,Hanjia Zheng, Agosh Saini,Fatemeh Bakhshandeh,Fatemeh Keyvani, Dragos Mantaila,Fasih A. Rahman,Joe Quadrilatero,Leyle Soleymani,Mahla Poudineh
Advanced Sensor Researchno. 3 (2024): n/a-n/a
Eric A. Lee,Leonard Angka, Sarah-Grace Rota, Thomas Hanlon,Andrew Mitchell,Rose Hurren,Xiao Ming Wang,Marcela Gronda,Ezel Boyaci,Barbara Bojko,Mark Minden, Shrivani Sriskanthadevan,
crossref(2023)
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