The predictice valve of combining sarcopenia and clinical muti-pramater for postoperative complications of colorectal cancer patients
Ontology highlight
ABSTRACT:
DISEASE(S): Sarcopenia, Colorectal Cancer
PROVIDER: 88331 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:Background and aims: Insulin-like growth factor 2 (IGF2) is closely associated with the occurrence and development of primary and secondary muscle atrophy. This study investigates the role of IGF2 deficiency in inducing muscle atrophy using muscle-specific Igf2 knockout mice, aiming to provide theoretical basis and new concepts for growth hormone supplementation therapy in muscle atrophy. Methods: We analyzed Igf2 expression using the Tabula Muris single-cell database and generated muscle-specific Igf2 knockout mice using the Cre/LoxP system with Mck-cre transgenic mice. We characterized the phenotype and assessed muscle size and mass through external observation, dissection, H&E staining, and microCT scanning. Muscle function was evaluated using the Md3000 grip strength meter, treadmill tests for endurance and electromyography (EMG) for contraction force. Transcriptome sequencing was performed on muscle tissues to analyze the impact of Igf2 deletion on gene expression and pathways. Results: The Tabula Muris database confirmed high Igf2 expression in limb muscles, and we successfully developed muscle-specific Igf2 knockout (Igf2 cKO) mice. Analyses using MicroCT and H&E staining showed reduced muscle size, weight, and density in the gastrocnemius of Igf2 cKO mice versus controls. Grip strength tests using the Md3000 animal grip strength meter and treadmill tests assessing running endurance both indicated reduced physical performance in the Igf2 cKO group, with weakened grip strength and decreased running endurance distance and time. Electromyography (EMG) measurements disclosed a decrease in gastrocnemius muscle contraction force in the Igf2 cKO group. Transcriptome sequencing highlighted significant functional changes in muscle-related processes, RNA polymerase II transcription, and the PI3K pathway in the Igf2 cKO mice. Conclusions: Igf2 is highly expressed in skeletal muscle tissue. Muscle-specific Igf2 knockout mice exhibited reduced muscle size, weight, and density, weakened grip strength, decreased gastrocnemius muscle contraction force, and reduced running endurance distance and time. These findings suggest that IGF2 supplementation may be a potentially effective strategy for treating muscle atrophy.
2025-12-01 | GSE281658 | GEO
Project description:Frailty in elderly cardiovascular disease (CVD) patients is linked to declining functional capacity and procedural complications. This study investigated the transcriptomic signature of frailty in patients ≥70 years undergoing cardiac surgery or TAVI. Frailty was assessed using mobility, gait speed, and handgrip strength. Muscle samples were collected during surgery for RNA sequencing, and gene expression was analyzed. Transcriptomic analysis identified 10 frailty-associated genes, with S100A1 showing the strongest association. Functional studies confirmed S100A1’s role in muscle function, and higher blood S100A1 levels correlated with handgrip strength in a second cohort. S100A1 is a potential target for addressing frailty in elderly CVD patients and offers insights into genetic factors contributing to frailty.
2025-06-16 | GSE287726 | GEO
Project description:In today's 24/7 society, circadian misalignment caused by environmental and lifestyle factors is associated with various adverse health consequences, underscoring the need to understand tissue-specific pathology. A potential association of environmental circadian misalignment with sarcopenia, or accelerated loss of skeletal muscle strength and mass, is poorly documented. Here, we exposed wild-type C57BL/6J male mice to a chronic (64 weeks) jet lag (CJL) paradigm. CJL caused significant reductions in muscle strength and weight relative to untreated mice. Transcriptomic and histological analysis showed activation of TWEAK/Fn14 signaling and reduced myofiber cross-sectional area, hallmark features of sarcopenia. Furthermore, CJL mice showed increased centrally nucleated fibers, myosin heavy chain co-expressing fibers, and myogenic gene expression, suggesting that insufficient muscle regeneration likely contributes to muscle atrophy. These findings demonstrate that circadian misalignment is an independent risk factor for sarcopenia, underscoring circadian rhythms as a key regulator and actionable target for sarcopenia prevention.
2025-12-09 | GSE296198 | GEO
Project description:Interventions: Experimental group:nutrition and exercise investigation and Intervention;Control Group:nutrition and exercise investigation
Primary outcome(s): Skeletal muscle mass and strength;Nutrition assessment;physical examination
Study Design: Case-Control study
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Project description:AbstractBackground: A decreased intramuscular carnitine status with aging may contribute to frailty and fatigue, but studies are often confounded by sex-heterogeneity and lack of control groups. We hypothesize that muscle carnitine deficiency is associated with (pre-)frailty, diminished physical performance and altered mitochondrial function, possibly in a sex-dependent manner. This was tested in well-matched age groups, allowing gender-specific analyses. Methods: A cross-sectional study was performed in well-matched fit (n = 15) and (pre-)frail (n = 13) old males as well as in fit (n = 15) and (pre-)frail (n = 11) old females, using young males (n = 13) and females (n = 13) as healthy controls. In the elderly, frailty was assessed according to the Fried criteria and physical performance was determined by 400-m walk test, short physical performance battery and handgrip strength. Acylcarnitine status was assessed in muscle biopsies and blood plasma using liquid chromatography-tandem mass spectrometry. Muscle mitochondrial gene expression was analyzed. Results: Intramuscular total carnitine levels and short chain acylcarnitine levels were lower in (pre-)frail old females compared to fit old females and young females, whereas no differences were observed in males. Intramuscular short chain acylcarnitine levels were associated with low physical performance in females, even after correction for muscle mass (%), whereas in males no such association was found. The decline in short chain acylcarnitine levels in (pre-)frail old females was associated with low expression of genes involved in mitochondrial energy production and mitochondrial functionality. Conclusions: In (pre-)frail old females, intramuscular total carnitine levels and short chain acylcarnitine levels are decreased and this decrease is accompanied by reduced physical performance and low expression of a wide range of genes involved in mitochondrial function.
2023-02-04 | GSE144304 | GEO
Project description:D-galactose (D-gal) is a widely used chemical to induce cellular senescence. Cells undergoing senescence induced by D-gal exhibit mitochondrial structural damage and a decline in energy metabolism, which are highly related to cellular aging Studies have confirmed that D-gal can induce senescence, fibrosis, and redox imbalance in skeletal muscle fibroblasts. Our results confirm that D-galactose effectively induces cellular senescence and skeletal muscle fibrosis in both cellular and animal models. The increase in senescence markers and fibrosis-related proteins, along with the observed decline in muscle strength and mass, are consistent with previous studies that highlight the role of D-galactose in modeling aging-associated pathologies. The observed lethargy and reduction in muscle fiber cross-sectional area further validate the model's relevance to sarcopenia research.
2025-01-09 | GSE285869 | GEO
Project description:Genome wide DNA methylation profiling of muscle tissue genomic DNA. The Illumina Infinium MethylationEPIC array was used to obtain DNA methylation profiles across approximately 850,000 CpGs. Samples were male, taken from both the Hertfordshire Sarcopenia Study (HSS, n=34) and the Hertfordshire Sarcoepnia Study exension (HSSe, n=44), to determine DNA methylation associations with measures of muscle mass and function. We further aimed to test whether differences in the muscle methylome are associated with sarcopenia in older individuals. We found significant associations between DNA methylation in the muscle tissue and sarcopenia, as well as individual measures of muscle mass and function, enriched around EZH2 binding sites.
2021-12-15 | GSE154980 | GEO
Project description:Abstract Background: The prevalence of sarcopenia is increasing and effective interventions are required to prevent or reverse age-related muscle loss. However it is often challenging expensive and time-consuming to develop and test the effectiveness of such interventions. Furthermore translational animal models that adequately mimic underlying physiological pathways are scarce. Strong predictors for the incidence of sarcopenia include a sedentary life-style and malnutrition. Therefore our objective was to investigate the translational value of three potential mouse models for sarcopenia namely partial immobilized caloric restricted (CR) and a combination (immobilized & CR) model. Methods: C57BL/6J mice were calorically restricted (-40%) and/or one hindleg was immobilized for two weeks to induce loss of muscle mass and function. Muscle mass function and diameter and distribution of slow (type 1) and fast ( type 2) myofibers were compared to those of young control (4 months) and old reference mice (21 months). Transcriptome analysis of quadriceps muscle was performed to identify underlying pathways and were compared with those being expressed in aged human vastus lateralis muscle-biopsies using a meta-analysis of five different human studies. Results: Caloric restriction induced overall loss of lean body mass (-15% p<0.001) whereas immobilization decreased muscle strength (-28% p<0.001) and muscle mass of hindleg muscles specifically (on average -25% p<0.001). The proportion of slow myofibers increased with aging in mice (+5% p<0.05) and this was not recapitulated by the CR and/or immobilization models. The diameter of fast myofibers decreased with aging (-7% p<0.05) and this was mimicked by all models. Transcriptome analysis revealed that the combination of CR and immobilization recapitulated more pathways characteristic for human muscle-aging (73%) than naturally aged (21 months old) mice (45%). These pathways included critical pathways relevant for protein synthesis/ breakdown (mitochondrial) metabolism neurology and the vascular system. Conclusions: The combination model exhibits loss of both muscle mass (due to CR) and function (due to immobilization) and has a remarkable similarity with pathways underlying human sarcopenia. Our results demonstrate that naturally aging up to 21 months in mice only partially recapitulates the human pathology with fewer overlapping pathways than the combination model. These findings underline that external factors such as sedentary behavior and malnutrition are key elements of a translational mouse model and favor the combination model as a rapid model for testing the treatments against sarcopenia.
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