Special Issue "Myostatin in Aging and Disease"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (10 February 2021).

Special Issue Editor

Dr. Christopher Fry
E-Mail Website
Guest Editor
Department of Athletic Training and Clinical Nutrition, University of Kentucky, Lexington, United States
Interests: skeletal muscle adaptation; TGF-β signaling; extracellular matrix organization; fibro/adipogenic progenitor cells; satellite cells; sarcopenia

Special Issue Information

Dear Colleagues,

Myostatin, also known as growth and differentiation factor 8 (GDF8), is a member of the transforming growth factor β (TGF‐β) superfamily. Myostatin is primarily expressed in skeletal muscle, where it acts as a negative regulator of muscle growth and development, and has long been linked to muscle wasting disorders. Much work has elucidated downstream signalling following the binding of activated myostatin to the activin type II receptor to effect change in muscle size, in addition to metabolic adaptations. Given the prominent role for myostatin in the regulation of muscle size, as well its impact on metabolism and function of neighbouring tissues, myostatin shows great promise as a therapeutic target. Elevations in myostatin expression have been suggested to participate in muscle wasting during disuse, cancer, ageing, liver disease, end stage renal disease, COPD, and numerous other acute and chronic catabolic conditions. However, recent results from clinical trials of myostatin inhibitors have somewhat challenged the early promise of myostatin inhibition-based therapies. More recent work has also begun to dissect many of the molecular mechanisms whereby myostatin alters neighbouring tissues as a myokine. These include but are not limited to osteoblastic differentiation, obesity development, insulin resistance, fibrotic processes, and local and systemic inflammation. For these reasons, a greater understanding of myostatin induction, regulation, and overall function is needed to dissect and validate myostatin as a prognostic biomarker and therapeutic target for treating muscle and metabolic diseases. This Special Issue of Cells will improve our understanding of how myostatin contributes to skeletal muscle metabolism; ageing; and, ultimately, disease pathology. Given the conservation of the myostatin gene across several animal species, including vertebrate and invertebrate, submissions are welcome from those studying model organisms.

We are looking forward to your contributions to this Special Issue.

Dr. Christopher Fry
Guest Editor

Manuscript Submission Information

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Keywords

  • regulation of gene expression
  • skeletal muscle atrophy and catabolism
  • cellular signaling transduction
  • insulin resistance and metabolic imbalance
  • bone formation

Published Papers (2 papers)

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Open AccessReview
Antimyostatin Treatment in Health and Disease: The Story of Great Expectations and Limited Success
Cells 2021, 10(3), 533; https://doi.org/10.3390/cells10030533 - 03 Mar 2021
Viewed by 350
Abstract
In the past 20 years, myostatin, a negative regulator of muscle mass, has attracted attention as a potential therapeutic target in muscular dystrophies and other conditions. Preclinical studies have shown potential for increasing muscular mass and ameliorating the pathological features of dystrophic muscle [...] Read more.
In the past 20 years, myostatin, a negative regulator of muscle mass, has attracted attention as a potential therapeutic target in muscular dystrophies and other conditions. Preclinical studies have shown potential for increasing muscular mass and ameliorating the pathological features of dystrophic muscle by the inhibition of myostatin in various ways. However, hardly any clinical trials have proven to translate the promising results from the animal models into patient populations. We present the background for myostatin regulation, clinical and preclinical results and discuss why translation from animal models to patients is difficult. Based on this, we put the clinical relevance of future antimyostatin treatment into perspective. Full article
(This article belongs to the Special Issue Myostatin in Aging and Disease)
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The Failed Clinical Story of Myostatin Inhibitors against Duchenne Muscular Dystrophy: Exploring the Biology behind the Battle
Cells 2020, 9(12), 2657; https://doi.org/10.3390/cells9122657 - 10 Dec 2020
Cited by 3 | Viewed by 983
Abstract
Myostatin inhibition therapy has held much promise for the treatment of muscle wasting disorders. This is particularly true for the fatal myopathy, Duchenne Muscular Dystrophy (DMD). Following on from promising pre-clinical data in dystrophin-deficient mice and dogs, several clinical trials were initiated in [...] Read more.
Myostatin inhibition therapy has held much promise for the treatment of muscle wasting disorders. This is particularly true for the fatal myopathy, Duchenne Muscular Dystrophy (DMD). Following on from promising pre-clinical data in dystrophin-deficient mice and dogs, several clinical trials were initiated in DMD patients using different modality myostatin inhibition therapies. All failed to show modification of disease course as dictated by the primary and secondary outcome measures selected: the myostatin inhibition story, thus far, is a failed clinical story. These trials have recently been extensively reviewed and reasons why pre-clinical data collected in animal models have failed to translate into clinical benefit to patients have been purported. However, the biological mechanisms underlying translational failure need to be examined to ensure future myostatin inhibitor development endeavors do not meet with the same fate. Here, we explore the biology which could explain the failed translation of myostatin inhibitors in the treatment of DMD. Full article
(This article belongs to the Special Issue Myostatin in Aging and Disease)
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