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In semelparous species like the ayu (), spawning is followed by rapid physiological decline and death; yet, the underlying molecular mechanisms remain largely unexplored. This study examines transcriptomic changes in ayu skeletal muscle before and after spawning, with a focus on key genes and pathways contributing to muscle atrophy and metabolic dysfunction. Through RNA sequencing and DEG analysis, we identified over 3000 DEGs, and GSEA and KEGG pathway analysis revealed significant downregulation of energy metabolism and protein degradation. In post-spawning ayu, a rapid decrease in body weight was observed, accompanied by a decline in the expression of myosin heavy chain genes, which are major muscle protein genes, and gene expression changes indicative of muscle atrophy. Decreased expression of AP-1 transcription factors associated with muscle development and aging was also evident. PPI network analysis identified carbohydrate catabolism protein gapdh may be the key factor that led to muscle atrophy and accelerated aging in ayu. Our study revealed that after spawning, the ayu muscle tissue undergoes strong metabolic disorders and cellular stress responses, providing special insights into the mechanisms through the post-spawning death of ayu.
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http://dx.doi.org/10.3390/ijms26020434 | DOI Listing |
PLoS One
September 2025
Neck-Shoulder and Lumbocrural Pain Hospital of Shandong First Medical University, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, China.
Background: Metabolic syndrome (MetS) and sarcopenia are major global public health problems, and their coexistence significantly increases the risk of death. In recent years, this trend has become increasingly prominent in younger populations, posing a major public health challenge. Numerous studies have regarded reduced muscle mass as a reliable indicator for identifying pre-sarcopenia.
View Article and Find Full Text PDFJ Clin Invest
September 2025
Department of Genetics, Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan.
Few drugs are available for rare diseases due to economic disincentives. However, tailored medications for extremely-rare disorders (N-of-1) offer a ray of hope. Artificial antisense oligonucleotides (ASOs) are now best known for their use in spinal muscular atrophy (SMA).
View Article and Find Full Text PDFJCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
View Article and Find Full Text PDFJ Oral Rehabil
September 2025
Division of Functional Oral Neuro Science, Graduate School of Dentistry, The University of Osaka, Osaka, Japan.
Background: Older adults have decreased swallowing-related muscle mass, which may lead to decreased swallowing function. One of the causes of this decrease in muscle mass in older adults is a decrease in swallowing frequency.
Objective: The purpose of this study was to evaluate the relationship between swallowing frequency and swallowing-related muscle mass.
Mol Genet Genomic Med
September 2025
Department of Maternal-Fetal Medicine, Augusta University, Augusta, Georgia, USA.
Introduction: Spinal muscular atrophy (SMA), caused by pathogenic variants in the survival motor neuron (SMN) gene, is the most common genetic cause of mortality in children under the age of two. Prior reports of obstetric sonograms performed in pregnancies with severe forms of fetal SMA have discrepant findings that may stem from a failure to account for the SMN2 copy number.
Methods: We present a neonate diagnosed with SMA type 0 postnatally (0SMN1/1SMN2 genotype).