ArticleInternational journal of oncology2013
Altered cardiac muscle mTOR regulation during the progression of cancer cachexia in the ApcMin/+ mouse.
Article in International journal of oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 54 citations in OpenAlex.
- Thbs1Journal of advanced research · 2026Article
- Chemotherapy-induced cardiotoxicity in breast cancer: mechanisms, diagnostic advances, and emerging protective strategies.American journal of physiology. Heart and circulatory physiology · 2025Review
- Early Markers of Cardiac and Skeletal Muscle Metabolic Derangement in the Apc(min/+) Male Mouse.Cancer reports (Hoboken, N.J.) · 2025Article
- Establishment and characterization of novel cancer cachexia-inducing cell line, Aku60GC, of scirrhous gastric cancer.Human cell · 2025Article
- Anabolic deficits and divergent unfolded protein response underlie skeletal and cardiac muscle growth impairments in the Yoshida hepatoma tumor model of cancer cachexia.Physiological reports · 2024Article
- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Cardiac Remodeling in Cancer-Induced Cachexia: Functional, Structural, and Metabolic Contributors.Cells · 2022Review
- Review
- Pathological features of tissues and cell populations during cancer cachexia.Cell regeneration (London, England) · 2022Review
- Review
- Cardiac Complications: The Understudied Aspect of Cancer Cachexia.Cardiovascular toxicology · 2022Review
- Cardioprotective effects of preconditioning exercise in the female tumor bearing mouse.Frontiers in cell and developmental biology · 2022Article
- Nutrition challenges of cancer cachexia.JPEN. Journal of parenteral and enteral nutrition · 2021Review
- Anthracycline-free tumor elimination in mice leads to functional and molecular cardiac recovery from cancer-induced alterations in contrast to long-lasting doxorubicin treatment effects.Basic research in cardiology · 2021Article
- The Role of Autophagy Modulated by Exercise in Cancer Cachexia.Life (Basel, Switzerland) · 2021Review
- The Role of Tumor Microenvironment Cells in Colorectal Cancer (CRC) Cachexia.International journal of molecular sciences · 2021Review
- Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia.Oncogenesis · 2021Review
- ACVR2B antagonism as a countermeasure to multi-organ perturbations in metastatic colorectal cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2020Article
- Diverging metabolic programmes and behaviours during states of starvation, protein malnutrition, and cachexia.Journal of cachexia, sarcopenia and muscle · 2020Review
- Molecular mechanisms of cancer cachexia‑induced muscle atrophy (Review).Molecular medicine reports · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer cachexia is a muscle wasting condition that occurs in response to a malignant growth in the body. The mechanisms regulating cardiac muscle mass with cachexia are not well understood. Using the ApcMin/+ mouse model of colorectal cancer, we investigated how cachexia affects the regulation of 5'-adenosine monophosphate-activated protein kinase (AMPK), protein kinase B (Akt) and mammalian target of rapamycin (mTOR) signaling in the heart. Compared to age-matched C57BL/6 (BL6) mice, ApcMin/+ body mass and heart mass were lower at 12 (11 ± 5 and 8 ± 3%, respectively) and 20 weeks (26 ± 3 and 6 ± 4%, respectively) of age (P<0.05). Diminished heart mass in the 20-week-old ApcMin/+ mice coincided with a decreased rate of myofibrillar protein synthesis and increased AMPKα phosphorylation. Cachexia decreased mTOR phosphorylation and the phosphorylation of the mTOR substrates, S6 ribosomal protein and 4EBP1 independent of Akt activation. These changes in mTOR-related protein signaling were accompanied by modest increases in the amount of Beclin1 but not protein ubiquitination or cardiomyocyte apoptosis. Taken together, these data suggest that loss of cardiac mass during cachexia progression in the ApcMin/+ mouse is associated with an Akt-independent suppression of anabolic signaling and evidence of increased autophagy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.