ArticleScientific reports2019
Inhibition of activin-like kinase 4/5 attenuates cancer cachexia associated muscle wasting.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Novel high throughput 3D ECM remodeling assay identifies MEK as key driver of fibrotic fibroblast activity.Materials today. Bio · 2025Article
- Molecular mechanisms of cancer cachexia-related loss of skeletal muscle mass: data analysis from preclinical and clinical studies.Journal of cachexia, sarcopenia and muscle · 2023Review
- Muscle and Bone Defects in Metastatic Disease.Current osteoporosis reports · 2022Review
- Genetic Disruption of Guanylyl Cyclase/Natriuretic Peptide Receptor-A Triggers Differential Cardiac Fibrosis and Disorders in Male and Female Mutant Mice: Role of TGF-β1/SMAD Signaling Pathway.International journal of molecular sciences · 2022Article
- Article
- Effects of TGF-β1 Receptor Inhibitor GW788388 on the Epithelial to Mesenchymal Transition of Peritoneal Mesothelial Cells.International journal of molecular sciences · 2021Article
- Phenotypic features of cancer cachexia-related loss of skeletal muscle mass and function: lessons from human and animal studies.Journal of cachexia, sarcopenia and muscle · 2021Review
- Review
- Receptor binding competition: A paradigm for regulating TGF-β family action.Cytokine & growth factor reviews · 2021Review
- Skeletal Muscle Deconditioning in Breast Cancer Patients Undergoing Chemotherapy: Current Knowledge and Insights From Other Cancers.Frontiers in cell and developmental biology · 2021Review
- Functional redundancy of type I and type II receptors in the regulation of skeletal muscle growth by myostatin and activin A.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Molecular mechanisms of cancer cachexia‑induced muscle atrophy (Review).Molecular medicine reports · 2020Review
- Muscle alterations in the development and progression of cancer-induced muscle atrophy: a review.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer mediated activation of the ActRIIB-ALK4/5 heterodimer by myostatin is strongly associated with muscle wasting. We investigated in vitro and in vivo the efficacy of ALK4/5 receptor blockers SB431542 and GW788388 in preventing muscle wasting, and explored synergy with IGF-I analogue LONG R3 (LR3) IGF-I. In vitro, C2C12 skeletal muscle cells were treated with vehicle, SB431542, GW788388 and LR3 IGF-I. A C26-CD2F1 cachexia model was used to induce cachexia in vivo. Mice were allocated as non-tumour bearing (NTB) or C26 tumour-bearing (C26 TB) vehicle control, treated with SB431542, LR3 IGF-I, SB431542 and LR3 IGF-I, or GW788388 (intraperitoneally or orally). In vitro, differentiation index and mean nuclei count increased using SB431542, GW788388, LR3 IGF-I. In vivo, GW788388 was superior to SB431542 in limiting loss of bodyweight, grip-strength and gastrocnemius weight. and downregulated Atrogin-1 expression comparable to NTB mice. LR3 IGF-I treatment limited loss of muscle mass, but at the expense of accelerated tumour growth. In conclusion, treatment with GW788388 prevented cancer cachexia, and downregulated associated ubiquitin ligase Atrogin-1.
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