The INSR/AKT/mTOR pathway regulates the pace of myogenesis in a syndecan-3-dependent manner

Jones, Fiona K.; Jones, Andrew R.; Pisconti, Addolorata

doi:10.1016/j.matbio.2022.09.004

Cited by 2 publications

(1 citation statement)

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“…Syndecans are involved in several signaling pathways, including ERK/MAPK ( Hara et al, 2021 ), AKT/mTOR/S6K1, and Wnt signaling ( Luyten et al, 2008 ; Jones et al, 2020 ; Hara et al, 2021 ; Johnson de Sousa Brito et al, 2021 ; Jones et al, 2022 ); however, none of them have previously been investigated in the context of WB myopathy.…”

Section: Discussionmentioning

confidence: 99%

Characterization of wooden breast myopathy: a focus on syndecans and ECM remodeling

Pejšková,

Rønning,

Kent

et al. 2023

Front. Physiol.

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Introduction: The skeletal muscle deformity of commercial chickens (Gallus gallus), known as the wooden breast (WB), is associated with fibrotic myopathy of unknown etiology. For future breeding strategies and genetic improvements, it is essential to identify the molecular mechanisms underlying the phenotype. The pathophysiological hallmarks of WB include severe skeletal muscle fibrosis, inflammation, myofiber necrosis, and multifocal degeneration of muscle tissue. The transmembrane proteoglycans syndecans have a wide spectrum of biological functions and are master regulators of tissue homeostasis. They are upregulated and shed (cleaved) as a regulatory mechanism during tissue repair and regeneration. During the last decades, it has become clear that the syndecan family also has critical functions in skeletal muscle growth, however, their potential involvement in WB pathogenesis is unknown.Methods: In this study, we have categorized four groups of WB myopathy in broiler chickens and performed a comprehensive characterization of the molecular and histological profiles of two of them, with a special focus on the role of the syndecans and remodeling of the extracellular matrix (ECM).Results and discussion: Our findings reveal differential expression and shedding of the four syndecan family members and increased matrix metalloproteinase activity. Additionally, we identified alterations in key signaling pathways such as MAPK, AKT, and Wnt. Our work provides novel insights into a deeper understanding of WB pathogenesis and suggests potential therapeutic targets for this condition.

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Section: Discussionmentioning

confidence: 99%

Characterization of wooden breast myopathy: a focus on syndecans and ECM remodeling

Pejšková,

Rønning,

Kent

et al. 2023

Front. Physiol.

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The Role of Mitochondria in Mediation of Skeletal Muscle Repair

Paez

Pitzer

2023

Muscles

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Musculoskeletal health is directly linked to independence and longevity, but disease and aging impairs muscle mass and health. Complete repair after a pathological or physiological muscle injury is critical for maintaining muscle function, yet muscle repair is compromised after disuse, or in conditions such as metabolic diseases, cancer, and aging. Regeneration of damaged tissue is critically dependent upon achieving the optimal function of satellite cells (muscle stem cells, MSCs). MSC remodeling in muscle repair is highly dependent upon its microenvironment, and metabolic health of MSCs, which is dependent on the functional capacity of their mitochondria. Muscle repair is energy demanding and mitochondria provide the primary source for energy production during regeneration. However, disease and aging induce mitochondrial dysfunction, which limits energy production during muscle regeneration. Nevertheless, the role of mitochondria in muscle repair likely extends beyond the production of ATP and mitochondria could provide potentially important regulatory signaling to MSCs during repair from injury. The scope of current research in muscle regeneration extends from molecules to exosomes, largely with the goal of understanding ways to improve MSC function. This review focuses on the role of mitochondria in skeletal muscle myogenesis/regeneration and repair. A therapeutic strategy for improving muscle mitochondrial number and health will be discussed as a means for enhancing muscle regeneration. Highlights: (a). Mitochondrial dysfunction limits muscle regeneration; (b). Muscle stem cell (MSC) function can be modulated by mitochondria; (c). Enhancing mitochondria in MSCs may provide a strategy for improving muscle regeneration after an injury.

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The INSR/AKT/mTOR pathway regulates the pace of myogenesis in a syndecan-3-dependent manner

Cited by 2 publications

References 76 publications

Characterization of wooden breast myopathy: a focus on syndecans and ECM remodeling

Characterization of wooden breast myopathy: a focus on syndecans and ECM remodeling

The Role of Mitochondria in Mediation of Skeletal Muscle Repair

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