David W. Hammers
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View article: Functional and structural pathologies in skeletal muscle of a rat model of Duchenne muscular dystrophy
Functional and structural pathologies in skeletal muscle of a rat model of Duchenne muscular dystrophy Open
Background Duchenne muscular dystrophy (DMD) is a lethal pediatric degenerative muscle disease for which there is no cure. Robust preclinical models that recapitulate major clinical features of DMD are required to investigate efficacy of p…
View article: Dual S100A1 and ARC gene therapy as a treatment for DMD cardiomyopathy
Dual S100A1 and ARC gene therapy as a treatment for DMD cardiomyopathy Open
Duchenne muscular dystrophy (DMD) is a lethal pediatric striated muscle disease caused by loss of dystrophin for which there is no cure. Cardiomyopathy is the leading cause of death amongst individuals with DMD, and effective therapeutics …
View article: Effect of Tadalafil on cardiac function and left ventricular dimensions in Duchenne muscular dystrophy: safety and cardiac MRI substudy results from a randomized, placebo-controlled trial
Effect of Tadalafil on cardiac function and left ventricular dimensions in Duchenne muscular dystrophy: safety and cardiac MRI substudy results from a randomized, placebo-controlled trial Open
View article: Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice
Comparative lipidomic and metabolomic profiling of mdx and severe mdx-apolipoprotein e-null mice Open
Despite its notoriously mild phenotype, the dystrophin-deficient mdx mouse is the most common model of Duchenne muscular dystrophy (DMD). By mimicking a human DMD-associated metabolic comorbidity, hyperlipidemia, in mdx mice by inactivatin…
View article: Spatiotemporal transcriptomic mapping of regenerative inflammation in skeletal muscle reveals a dynamic multilayered tissue architecture
Spatiotemporal transcriptomic mapping of regenerative inflammation in skeletal muscle reveals a dynamic multilayered tissue architecture Open
Tissue regeneration is orchestrated by macrophages that clear damaged cells and promote regenerative inflammation. How macrophages spatially adapt and diversify their functions to support the architectural requirements of actively regenera…
View article: Potential limitations of microdystrophin gene therapy for Duchenne muscular dystrophy
Potential limitations of microdystrophin gene therapy for Duchenne muscular dystrophy Open
Clinical trials delivering high doses of adeno-associated viruses (AAVs) expressing truncated dystrophin molecules (microdystrophins) are underway for Duchenne muscular dystrophy (DMD). We examined the efficiency and efficacy of this strat…
View article: Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration
Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration Open
View article: Blocking muscle wasting via deletion of the muscle-specific E3 ligase MuRF1 impedes pancreatic tumor growth
Blocking muscle wasting via deletion of the muscle-specific E3 ligase MuRF1 impedes pancreatic tumor growth Open
Cancer-induced muscle wasting reduces quality of life, complicates or precludes cancer treatments, and predicts early mortality. Herein, we investigate the requirement of the muscle-specific E3 ubiquitin ligase, MuRF1, for muscle wasting i…
View article: Blocking muscle wasting via deletion of the muscle-specific E3 ubiquitin ligase MuRF1 impedes pancreatic tumor growth
Blocking muscle wasting via deletion of the muscle-specific E3 ubiquitin ligase MuRF1 impedes pancreatic tumor growth Open
Cancer-induced muscle wasting reduces quality of life, complicates or precludes cancer treatments, and predicts early mortality. Herein, we investigated the requirement of the muscle-specific E3 ubiquitin ligase, MuRF1, for muscle wasting …
View article: Magnetic resonance quantification of skeletal muscle lipid infiltration in a humanized mouse model of Duchenne muscular dystrophy
Magnetic resonance quantification of skeletal muscle lipid infiltration in a humanized mouse model of Duchenne muscular dystrophy Open
Rodent models of Duchenne muscular dystrophy (DMD) often do not recapitulate the severity of muscle wasting and resultant fibro‐fatty infiltration observed in DMD patients. Having recently documented severe muscle wasting and fatty deposit…
View article: NOX4 inhibition promotes the remodeling of dystrophic muscle
NOX4 inhibition promotes the remodeling of dystrophic muscle Open
The muscular dystrophies (MDs) are genetic muscle diseases that result in progressive muscle degeneration followed by the fibrotic replacement of affected muscles as regenerative processes fail. Therapeutics that specifically address the f…
View article: Potential limitations of micro-dystrophin gene therapy for Duchenne muscular dystrophy
Potential limitations of micro-dystrophin gene therapy for Duchenne muscular dystrophy Open
Adeno-associated viruses (AAVs) expressing versions of truncated dystrophin (micro-dystrophins) are being delivered at high doses to patients with Duchenne muscular dystrophy (DMD) in clinical trials. We examined this strategy with two dif…
View article: Evaluating Genetic Modifiers of Duchenne Muscular Dystrophy Disease Progression Using Modeling and MRI
Evaluating Genetic Modifiers of Duchenne Muscular Dystrophy Disease Progression Using Modeling and MRI Open
The results of this study link the historically mild phenotypes seen in individuals amenable to exon 8 skipping and with certain nonsense variations with alterations in trajectories of lower extremity muscle replacement by fat.
View article: The skeletal muscle circadian clock regulates titin splicing through RBM20
The skeletal muscle circadian clock regulates titin splicing through RBM20 Open
Circadian rhythms are maintained by a cell-autonomous, transcriptional–translational feedback loop known as the molecular clock. While previous research suggests a role of the molecular clock in regulating skeletal muscle structure and fun…
View article: Author response: The skeletal muscle circadian clock regulates titin splicing through RBM20
Author response: The skeletal muscle circadian clock regulates titin splicing through RBM20 Open
Article Figures and data Abstract Editor's evaluation Introduction Results Discussion Materials and methods Data availability References Decision letter Author response Article and author information Metrics Abstract Circadian rhythms are …
View article: Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration
Hedgehog signaling via its ligand DHH acts as cell fate determinant during skeletal muscle regeneration Open
Successful muscle regeneration relies on the interplay of multiple cell populations. However, the signals required for this coordinated intercellular crosstalk remain largely unknown. Here, we describe how the Hedgehog (Hh) signaling pathw…
View article: Evaluation of the DBA/2J mouse as a potential background strain for genetic models of cardiomyopathy
Evaluation of the DBA/2J mouse as a potential background strain for genetic models of cardiomyopathy Open
The potential use of the D2.mdx mouse (the mdx mutation on the DBA/2J genetic background) as a preclinical model of the cardiac aspects of Duchenne muscular dystrophy (DMD) has been criticized based on speculation that the DB…
View article: Evaluation of the DBA/2J mouse as a potential background strain for genetic models of cardiomyopathy
Evaluation of the DBA/2J mouse as a potential background strain for genetic models of cardiomyopathy Open
The potential use of the D2. mdx mouse (the mdx mutation on the DBA/2J genetic background) as a preclinical model of the cardiac aspects of Duchenne muscular dystrophy (DMD) has been criticized based on speculation that the DBA/2J genetic …
View article: NOX4 inhibition promotes the remodeling of dystrophic muscle
NOX4 inhibition promotes the remodeling of dystrophic muscle Open
The muscular dystrophies (MDs) are genetic muscle diseases that result in progressive muscle degeneration followed by the fibrotic replacement of affected muscles as regenerative processes fail. Therapeutics that specifically address the f…
View article: NF-κB modifies the mammalian circadian clock through interaction with the core clock protein BMAL1
NF-κB modifies the mammalian circadian clock through interaction with the core clock protein BMAL1 Open
In mammals, the circadian clock coordinates cell physiological processes including inflammation. Recent studies suggested a crosstalk between these two pathways. However, the mechanism of how inflammation affects the clock is not well unde…
View article: Filopodia powered by class x myosin promote fusion of mammalian myoblasts
Filopodia powered by class x myosin promote fusion of mammalian myoblasts Open
Skeletal muscle fibers are multinucleated cellular giants formed by the fusion of mononuclear myoblasts. Several molecules involved in myoblast fusion have been discovered, and finger-like projections coincident with myoblast fusion have a…
View article: Author response: Filopodia powered by class x myosin promote fusion of mammalian myoblasts
Author response: Filopodia powered by class x myosin promote fusion of mammalian myoblasts Open
View article: Filopodia powered by class X myosin promote fusion of mammalian myoblasts
Filopodia powered by class X myosin promote fusion of mammalian myoblasts Open
Skeletal muscle fibers are multinucleated cellular giants formed by the fusion of mononuclear myoblasts. Several molecules involved in myoblast fusion have been discovered, and finger-like projections coincident with myoblast fusion have a…
View article: The Skeletal Muscle Circadian Clock Regulates Titin Splicing Through RBM20
The Skeletal Muscle Circadian Clock Regulates Titin Splicing Through RBM20 Open
Circadian rhythms are maintained by a cell autonomous, transcriptional-translational feedback loop known as the molecular clock. While previous research suggests a role of the molecular clock in regulating skeletal muscle structure and fun…
View article: NF-κB modifies the mammalian circadian clock through interaction with the core clock protein BMAL1
NF-κB modifies the mammalian circadian clock through interaction with the core clock protein BMAL1 Open
In mammals, the circadian clock coordinates various cell physiological processes, including the inflammatory response. Recent studies suggested a crosstalk between these two pathways. However, the mechanism of how inflammation affects the …
View article: The D2.mdx mouse as a preclinical model of the skeletal muscle pathology associated with Duchenne muscular dystrophy
The D2.mdx mouse as a preclinical model of the skeletal muscle pathology associated with Duchenne muscular dystrophy Open
View article: Glucocorticoids counteract hypertrophic effects of myostatin inhibition in dystrophic muscle
Glucocorticoids counteract hypertrophic effects of myostatin inhibition in dystrophic muscle Open
Duchenne muscular dystrophy (DMD) is a devastating genetic muscle disease resulting in progressive muscle degeneration and wasting. Glucocorticoids, specifically prednisone/prednisolone and deflazacort, are commonly used by DMD patients. E…
View article: Functional muscle hypertrophy by increased insulin‐like growth factor 1 does not require dysferlin
Functional muscle hypertrophy by increased insulin‐like growth factor 1 does not require dysferlin Open
Introduction Dysferlin loss‐of‐function mutations cause muscular dystrophy, accompanied by impaired membrane repair and muscle weakness. Growth promoting strategies including insulin‐like growth factor 1 (IGF‐1) could provide benefit but m…
View article: Effects of PDE5 inhibition on dystrophic muscle following an acute bout of downhill running and endurance training
Effects of PDE5 inhibition on dystrophic muscle following an acute bout of downhill running and endurance training Open
Lack of sarcolemma-localized neuronal nitric oxide synthase mu (nNOSμ) contributes to muscle damage and fatigue in dystrophic muscle. In this study, we examined the effects of compensating for lack of nNOSμ with a phosphodiesterase type 5 …
View article: RevAMP(K)ing Mitochondria for Sarcoglycanopathy Therapeutics
RevAMP(K)ing Mitochondria for Sarcoglycanopathy Therapeutics Open