The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
Bone and morphogenetic protein signalling and muscle mass
Abstract
PURPOSE OF REVIEW: The purpose of this study is to discuss the involvement of bone and morphogenetic proteins (BMPs) in the control of muscle mass. RECENT FINDINGS: The transforming growth factor-beta (TGFβ) superfamily comprises a large number of secreted proteins that regulate a variety of fundamental biological processes. Sequence similarities define two ligand subfamilies: the TGFβ/Activin subfamily and the BMP subfamily. Within the members of TGFβ subfamily, myostatin emerged as the most critical ligand that affects muscle size and function. Indeed, mutations that inactivate Myostatin lead to important muscle growth in animals and humans. However, recent findings have increased the complexity of the TGFβ superfamily. Indeed, two independent groups have shown that BMP pathway, acting through Smad1/5/8, is the fundamental hypertrophic signal and dominates Myostatin signalling. Moreover, BMP-Smad1/5/8 negatively regulates a novel ubiquitin ligase, named MUSA1 that is required for muscle loss. This article reviews the rapid progress made in the last year regarding the signalling downstream TGFβ superfamily and its involvement in the homeostasis of adult muscle fibres. SUMMARY: The recent insights gained into the interplay of TGFβ and BMP signalling in muscle have challenged our pre-existing ideas of how the adult skeletal muscle phenotype is regulated in health and disease.
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“BMP pathway is activated in myostatin knockout and is sufficient, when induced, to promote muscle growth and to counteract muscle loss after denervation and in the absence of nutrients [6–8].”
From The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass (2021) · cites this paper as [8]
In the citing paper
“Mechanistically, muscle loss is due to FoxO-mediated activation of the ubiquitin–proteasome system together with the impairment of general autophagy and mitophagy pathways [25,31,32].”
From Inhibition of the Fission Machinery Mitigates OPA1 Impairment in Adult Skeletal Muscles (2019) · cites this paper as [32]
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Metadata
- Authors
- Sartori, R., & Sandri, M.
- Affiliations
- University of Padua (IT)
- Corresponding author
- Sandri, Marco
- Venue
- Current Opinion in Clinical Nutrition and Metabolic Care
- Published
- 2015-05
- Volume
- 18
- Issue
- 3
- Pages
- 215-220
- ISSN
- 1363-1950 (ISSN-L)
- OpenAlex
- W2076444039
- Cited by
- 22
- References
- 33
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 2 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 1 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 2
- FWCI
- 0.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Current Opinion in Clinical Nutrition & Metabolic Care (publishedVersion)
- PubMed (publishedVersion)
- Padua Research Archive (University of Padova) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- myostatin, TGF-beta superfamily, skeletal muscle mass, muscle hypertrophy, muscle atrophy, muscle growth
- MeSH terms
- Animals, Humans, Muscular Diseases, Signal Transduction, Transforming Growth Factor beta, Muscle, Skeletal, Bone Morphogenetic Proteins, Activins, Myostatin
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