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Rabbit meat constitutes a high-protein, low-fat nutritional resource demonstrating rising consumption, particularly within the Asia-Pacific region. Consequently, muscle growth and developmental pattern in meat rabbits represent critical economic considerations. To elucidate the primary signaling pathways governing muscle development, we first performed comparative body weight analyses between two rabbit breeds exhibiting divergent growth rates: the fast-growing Checkered Giant (Ju) and slow-growing Sichuan Ma rabbit. Subsequent, post-natal qualities of thigh and muscle fiber were quantified across three developmental phases (28, 56, and 84 days post-natal). The results showed the body weight of Ju rabbit was significantly higher than that of Ma rabbit beyond 3 weeks post-natal ( < 0.05), while Ma rabbit exhibited larger muscle fiber areas in both tissues at 56 days ( < 0.05). The transcriptome analysis showed that 284 and 305 differentially expressed genes (DEGs) (|log2FC| > 1, padj < 0.05) were identified in thigh muscle and muscle, respectively. GO (Gene Ontology) analysis of DEGs indicated DEGs in the thigh muscle were enriched in these terms related to biological processes of muscle cell migration and smooth muscle cell migration, cellular components of sarcomere, myofibril, and actin filament bundle, while DEGs in muscle were enriched in these terms associated with biological processes of muscle cell migration, smooth muscle cell migration and muscle structure development, cellular component of actin cytoskeleton, contractile fiber, myofibril, myosin complex and molecular function of actin filament binding. Integrated GO, KEGG and PPI analyses of co-expressive DEGs implicated the HIF-1 signaling pathway and Glycolysis/Gluconeogenesis in muscular development. Different expression of energy metabolism hub-genes might be the primary reason for interbreed muscle developmental disparities.
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http://dx.doi.org/10.3390/ani15111585 | DOI Listing |
Arterioscler Thromb Vasc Biol
September 2025
Vascular Biology Program, Boston Children's Hospital and Harvard Medical School, MA (K. Cui, B.Z., B.W., S.E.-B., A.V., H.C.).
Background: Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipid-laden foam cells and plaques within the arterial wall. Dysfunctional vascular smooth muscle cells (VSMCs), fibroblasts, endothelial cells, and macrophages contribute to disease progression. Here, we report that macrophage-specific expression of epsins, highly conserved endocytic adaptor proteins involved in clathrin-mediated endocytosis, accelerates atherosclerosis in Western diet-fed mice.
View Article and Find Full Text PDFVasc Specialist Int
September 2025
Department of Vascular Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
An abdominal aortic aneurysm (AAA) is defined as a localized dilation of the abdominal aorta measuring at least 1.5 times its normal diameter. If left untreated, AAA can progress to a life-threatening condition.
View Article and Find Full Text PDFACS Biomater Sci Eng
September 2025
Fischell Department of Bioengineering, University of Maryland, College Park, Maryland 20742, United States.
Uterine fibroids are the most common gynecological tumors, characterized by excessive production of extracellular matrix. Despite their prevalence, the cellular mechanisms governing fibroid growth remain poorly understood. Current in vitro models for fibroids do not replicate the complex 3D tissue mechanics, structure, and extracellular matrix components of fibroids, which may limit our understanding of fibroid pathogenesis.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
September 2025
Integrative Muscle Biology Laboratory, Division of Rehabilitation Sciences, College of Health Professions, University of Tennessee Health Science Center, Memphis, Tennessee, USA.
Background: Cancer promotes muscle wasting through an imbalance in the tightly regulated protein synthesis and degradation processes. An array of intracellular signalling pathways, including mTORC1 and AMPK, regulate protein synthesis, and these pathways are responsive to the muscle's microenvironment and systemic stimuli. Although feeding and fasting are established systemic regulators of muscle mTORC1 and protein synthesis, the cancer environment's impact on these responses during cachexia development is poorly understood.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
October 2025
Department of Surgery, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University, Maastricht, the Netherlands.
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