ArticleCell reports. Medicine2024
Oncostatin M signaling drives cancer-associated skeletal muscle wasting.
Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Transcriptomic response of skeletal muscle to acute aerobic versus combined exercise in chronic kidney disease.PloS one · 2026Trial
- Lipids grease the chain of cancer progression.Trends in cancer · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Skeletal muscle methylome-transcriptome disruptions during the onset and progression of colorectal cancer-induced cachexia.American journal of physiology. Cell physiology · 2026Article
- The canonical ER stress IRE1α/XBP1 pathway mediates skeletal muscle wasting during pancreatic cancer cachexia.EMBO molecular medicine · 2025Article
- Signaling networks governing skeletal muscle growth, atrophy, and cachexiaSkeletal muscle · 2025Review
- Cancer therapy and cachexia.The Journal of clinical investigation · 2025Review
- Article
- Exploring the Role of Inflammation and Metabolites in Bell's Palsy and Potential Treatment Strategies.Biomedicines · 2025Article
- Meeting report: the inaugural muscle biology and cachexia conference at the University of Houston, May 18-20, 2025, Houston, Texas, USA.Frontiers in physiology · 2025Article
- Exercise-mediated IL-6 downstream effects modulate brain pathology-can exercise training protocols influence the downstream effects?Frontiers in neurology · 2025Review
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- Transcriptional analysis of cancer cachexia: conserved and unique features across preclinical models and biological sex.American journal of physiology. Cell physiology · 2024Article
- Tumour-induced alterations in single-nucleus transcriptome of atrophying muscles indicate enhanced protein degradation and reduced oxidative metabolism.Journal of cachexia, sarcopenia and muscle · 2024Article
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
Progressive weakness and muscle loss are associated with multiple chronic conditions, including muscular dystrophy and cancer. Cancer-associated cachexia, characterized by dramatic weight loss and fatigue, leads to reduced quality of life and poor survival. Inflammatory cytokines have been implicated in muscle atrophy; however, available anticytokine therapies failed to prevent muscle wasting in cancer patients. Here, we show that oncostatin M (OSM) is a potent inducer of muscle atrophy. OSM triggers cellular atrophy in primary myotubes using the JAK/STAT3 pathway. Identification of OSM targets by RNA sequencing reveals the induction of various muscle atrophy-related genes, including Atrogin1. OSM overexpression in mice causes muscle wasting, whereas muscle-specific deletion of the OSM receptor (OSMR) and the neutralization of circulating OSM preserves muscle mass and function in tumor-bearing mice. Our results indicate that activated OSM/OSMR signaling drives muscle atrophy, and the therapeutic targeting of this pathway may be useful in preventing muscle wasting.
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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 Socratic graph.