Michael J. Bround
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View article: MCU-independent Ca2+ uptake mediates mitochondrial Ca2+ overload and necrotic cell death in a mouse model of Duchenne muscular dystrophy
MCU-independent Ca2+ uptake mediates mitochondrial Ca2+ overload and necrotic cell death in a mouse model of Duchenne muscular dystrophy Open
Mitochondrial Ca 2+ overload can mediate mitochondria-dependent cell death, a major contributor to several human diseases. Indeed, Duchenne muscular dystrophy (MD) is driven by dysfunctional Ca 2+ influx across the sarcolemma that causes m…
View article: MCUb is an inducible regulator of calcium-dependent mitochondrial metabolism and substrate utilization in muscle
MCUb is an inducible regulator of calcium-dependent mitochondrial metabolism and substrate utilization in muscle Open
Mitochondria use the electron transport chain to generate high-energy phosphate from oxidative phosphorylation, a process also regulated by the mitochondrial Ca2+ uniporter (MCU) and Ca2+ levels. Here, we show that MCUb, an inhibitor of MC…
View article: ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy
ANT-dependent MPTP underlies necrotic myofiber death in muscular dystrophy Open
Mitochondrial permeability transition pore (MPTP) formation contributes to ischemia-reperfusion injury in the heart and several degenerative diseases, including muscular dystrophy (MD). MD is a family of genetic disorders characterized by …
View article: MCUb Induction Protects the Heart From Postischemic Remodeling
MCUb Induction Protects the Heart From Postischemic Remodeling Open
Rationale: Mitochondrial Ca 2+ loading augments oxidative metabolism to match functional demands during times of increased work or injury. However, mitochondrial Ca 2+ overload also directly causes mitochondrial rupture and cardiomyocyte d…
View article: Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD
Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD Open
Genetic deletion of Ant1/2/4 and Ppif in mice inhibits the mitochondrial permeability transition pore.
View article: Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD
Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD Open
The mitochondrial permeability transition pore (MPTP) has resisted molecular identification for decades. The original model of the MPTP had the adenine nucleotide translocator (ANT) as the inner membrane pore-forming component. Indeed, rec…
View article: The mitochondrial calcium uniporter underlies metabolic fuel preference in skeletal muscle
The mitochondrial calcium uniporter underlies metabolic fuel preference in skeletal muscle Open
The mitochondrial Ca2+ uniporter (MCU) complex mediates acute mitochondrial Ca2+ influx. In skeletal muscle, MCU links Ca2+ signaling to energy production by directly enhancing the activity of key metabolic enzymes in the mitochondria. Her…
View article: Cardiac Ryanodine Receptor (Ryr2)-mediated Calcium Signals Specifically Promote Glucose Oxidation via Pyruvate Dehydrogenase
Cardiac Ryanodine Receptor (Ryr2)-mediated Calcium Signals Specifically Promote Glucose Oxidation via Pyruvate Dehydrogenase Open
Cardiac ryanodine receptor (Ryr2) Ca2+ release channels and cellular metabolism are both disrupted in heart disease. Recently, we demonstrated that total loss of Ryr2 leads to cardiomyocyte contractile dysfunction, arrhythmia, and reduced …
View article: The effects of RYR2 gene deletion on cardiac function and metabolism
The effects of RYR2 gene deletion on cardiac function and metabolism Open
The cardiac ryanodine receptor 2 (RYR2) is a sarcoplasmic reticulum Ca²⁺ release channel central to cardiomyocyte biology. RYR2 Ca²⁺ release has a well-established role in activating cardiomyocyte motor proteins during excitation-contracti…