ArticleeLife2024
Integrative study of skeletal muscle mitochondrial dysfunction in a murine pancreatic cancer-induced cachexia model.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Chemotherapy-Induced Skeletal Muscle Dysfunction and Cognitive Impairment: A Muscle-Brain Mechanistic Framework With Implications for Exercise Oncology.Journal of cachexia, sarcopenia and muscle · 2026Review
- Evaluative performance of triglyceride-glucose-frailty index versus surrogate insulin resistance indices for advanced cardiovascular-kidney-metabolic syndrome, cardiometabolic multimorbidity, and mortality: the role of estimated glomerular filtration rate.Cardiovascular diabetology · 2026Article
- The Secretome of a Cachexia-Inducing Lung Tumor Impairs Mitochondrial Function and Skeletal Muscle Differentiation.Cancers · 2026Article
- Sarcopenia as a Marker of Immunometabolic Vulnerability in Pancreatic Ductal Adenocarcinoma.Cancers · 2026Review
- Role of mitochondrial dysfunction in muscle wasting in cancer cachexia: a narrative review.Journal of translational medicine · 2026Review
- Correlation between oxidative stress and inflammation with metabolomics profile in skeletal muscle of ageing animal model and its modulation by tocotrienol-rich fraction.British journal of biomedical science · 2026Article
- Association between combined atherogenic and frailty index and cardiovascular events: evidence from the CHARLS cohort.Cardiovascular diabetology · 2025Article
- Impaired cAMP-PKA-CREB1 signalling drives mitochondrial dysfunction in skeletal muscle during cancer cachexia.Nature metabolism · 2025Article
- Cardiac atrophy associated to cancer: new perspectives in signaling pathways.Molecular biomedicine · 2025Article
- Exploring the potential of ginseng-derived compounds in treating cancer cachexia.Journal of ginseng research · 2025Review
- Review
- Histidine decarboxylase inhibition attenuates cancer-associated muscle wasting.The Journal of experimental medicine · 2025Article
- Predictive value of the combined triglyceride-glucose and frailty index for cardiovascular disease and stroke in two prospective cohorts.Cardiovascular diabetology · 2025Article
- Association of triglyceride-glucose index and its related parameters with functional disability: evidence from the China Health and Retirement Longitudinal Study.Frontiers in aging neuroscience · 2025Article
- Exploring the role of traditional Chinese medicine in sarcopenia: mechanisms and therapeutic advances.Frontiers in pharmacology · 2025Review
- Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC), the most common pancreatic cancer, is a deadly cancer, often diagnosed late and resistant to current therapies. PDAC patients are frequently affected by cachexia characterized by muscle mass and strength loss (sarcopenia) contributing to patient frailty and poor therapeutic response. This study assesses the mechanisms underlying mitochondrial remodeling in the cachectic skeletal muscle, through an integrative exploration combining functional, morphological, and omics-based evaluation of gastrocnemius muscle from KIC genetically engineered mice developing autochthonous pancreatic tumor and cachexia. Cachectic PDAC KIC mice exhibit severe sarcopenia with loss of muscle mass and strength associated with reduced muscle fiber's size and induction of protein degradation processes. Mitochondria in PDAC atrophied muscles show reduced respiratory capacities and structural alterations, associated with deregulation of oxidative phosphorylation and mitochondrial dynamics pathways. Beyond the metabolic pathways known to be altered in sarcopenic muscle (carbohydrates, proteins, and redox), lipid and nucleic acid metabolisms are also affected. Although the number of mitochondria per cell is not altered, mitochondrial mass shows a twofold decrease and the mitochondrial DNA threefold, suggesting a defect in mitochondrial genome homeostasis. In conclusion, this work provides a framework to guide toward the most relevant targets in the clinic to limit PDAC-induced cachexia.
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