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Limb muscle is responsible for physical activities and myogenic cell migration during embryogenesis is indispensable for limb muscle formation. Maternal obesity (MO) impairs prenatal skeletal muscle development, but the effects of MO on myogenic cell migration remain to be examined. C57BL/6 mice embryos were collected at E13.5. The GeoMx DSP platform was used to customize five regions along myogenic cell migration routes (myotome, dorsal/ventral limb, limb stroma, limb tip), and data were analyzed by GeomxTools 3.6.0. A total of 2224 genes were down-regulated in the MO group. The GO enrichment analysis showed that MO inhibited migration-related biological processes. The signaling pathways guiding myogenic migration such as hepatocyte growth factor signaling, fibroblast growth factor signaling, Wnt signaling and GTPase signaling were down-regulated in the MO E13.5 limb tip. Correspondingly, the expression levels of genes involved in myogenic cell migration, such as , , , and , were decreased in the MO group, especially in the dorsal and ventral sides of the limb. Additionally, myogenic differentiation-related genes were down-regulated in the MO limb. MO impedes myogenic cell migration and differentiation in the embryonic limb, providing an explanation for the impairment of fetal muscle development and offspring muscle function due to MO.
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http://dx.doi.org/10.3390/ijms25179488 | DOI Listing |
J Mol Histol
September 2025
Department of Urology, Yantai Yuhuangding Hospital, Qingdao University, No. 20 East Yuhuangding Road, Yantai, 264000, Shandong, China.
The stress urinary incontinence (SUI) is a difficulty in urology and current sub-urethral sling treatments are associated with inflamation and recurrence. In this study, we developed a novel tissue-engineered sling with myogenic induced adiposederived stem cells (MI-ADSCs) sheets induced by 5-Aza and combined with electrospun scaffolds of silk fibroin and poly(lactide-co-glycolide) (SF/PLGA) for the treatment of stress urinary incontinence. MI-ADSCs increased α-SMA, MyoD and Desmin the mRNA and protein expression.
View Article and Find Full Text PDFCalcif Tissue Int
September 2025
FirmoLab, Fondazione F.I.R.M.O. Onlus and Stabilimento Chimico Farmaceutico Militare (SCFM), 50141, Florence, Italy.
X-linked hypophosphatemia (XLH) is a rare and progressive disease, due to inactivating mutations in the phosphate-regulating endopeptidase homolog X-linked (PHEX) gene. These pathogenic variants result in elevated circulating levels of fibroblast growth factor 23 (FGF23), responsible for the main clinical manifestations of XLH, such as hypophosphatemia, skeletal deformities, and mineralization defects. However, XLH also involves muscular disorders (muscle weakness, pain, reduced muscle density, peak strength, and power).
View Article and Find Full Text PDFBioact Mater
December 2025
Department of Plastic Surgery, Peking University Third Hospital, Beijing, 100191, China.
Craniofacial muscles are essential for a variety of functions, including fine facial expressions. Severe injuries to these muscles often lead to more devastating consequences than limb muscle injuries, resulting in the loss of critical functions such as mastication and eyelid closure, as well as facial aesthetic impairment. Therefore, the development of targeted repair strategies for craniofacial muscle injuries is crucial.
View Article and Find Full Text PDFGenome Biol
September 2025
Department of Orthopaedics and Traumatology, The Chinese University of Hong Kong, Hong Kong SAR, China.
Background: DNA G-quadruplexes (G4s) are non-canonical secondary structures formed in guanine-rich DNA sequences and play important roles in modulating biological processes through a variety of gene regulatory mechanisms. Emerging G4 profiling allows global mapping of endogenous G4 formation.
Results: Here in this study, we map the G4 landscapes in adult skeletal muscle stem cells (MuSCs), which are essential for injury-induced muscle regeneration.
Genetic studies have linked (encoding soluble epoxide hydrolase, sEH) and (encoding cyclooxygenase-2, COX-2) to Alzheimer's disease (AD). Elevated levels of sEH and COX-2 found in AD patients and animals suggest their involvement in neurodegeneration, glial activation, vascular dysfunction, and inflammation. This study evaluated the effects of a new dual sEH/COX-2 inhibitor, PTUPB, on cerebrovascular function and cognition in TgF344-AD rats.
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