ArticleApoptosis : an international journal on programmed cell death2024
Myeloma extracellular vesicle-derived RAGE increases inflammatory responses and myotube atrophy in multiple myeloma through activation of the TLR4/NF-κB p65 pathway.
Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Targeting the AGE-RAGE/NF-κB Pathway: An Integrative Study Decoding the Anti-Colitis Effect of Five-Flavor Sophora Flavescens Enteric-Coated Capsule.Biomedicines · 2026Article
- Tumor-muscle communication in cancer-associated cachexia (Review).Oncology letters · 2026Review
- Lipoxin A4 activates Nrf2 expression and mitigates hyperglycaemia-induced impairment of myogenesis and rescues damage to mitochondria.Journal of physiology and biochemistry · 2026Article
- Mangiferin in human disease: Multifaceted mechanisms and applications (Review).International journal of molecular medicine · 2026Review
- Exercise-modulated IL-6 in cancer cachexia: molecular mechanisms and therapeutic potential.Journal of translational medicine · 2026Review
- Extracellular vesicles derived from pro-inflammatory M1 macrophages induce an inflammatory and invasive phenotype in melanoma cells.Cell communication and signaling : CCS · 2025Article
- The role of AGEs in skeletal muscle atrophy and the beneficial effects of exercise.Frontiers in medicine · 2025Review
- Therapeutically Harnessing Tumor Cell-Derived Extracellular Vesicles for Multiple Myeloma: Recent Advances and Future Perspectives.Pharmaceutics · 2024Review
- Overcoming drug resistance through extracellular vesicle-based drug delivery system in cancer treatment.Cancer drug resistance (Alhambra, Calif.) · 2024Review
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9 authors at 1 institution in 1 country.
Funding
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Abstract
Sarcopenia manifests as muscle atrophy and loss that is complicated with malignancy. This study explored the mechanism of extracellular vesicles (EVs) in multiple myeloma (MM) with sarcopenia. SP2/0 conditioned medium (CM) was collected to isolate SP2/0-EVs. C2C12 cells were incubated with SP2/0 CM or SP2/0-EVs. ROS, TNF-α, IL-6, MuRF1 and MyHC levels were detected by DCF-DA fluorescent probe, ELISA, and Western blot. GW4869 was used to inhibit EV secretion in SP2/0 to confirm its effect on muscle atrophy. Serum was collected from MM patients with or without sarcopenia to detect RAGE mRNA expression. SP2/0 cells were transfected with RAGE siRNA and C2C12 cells were treated with the isolated si-RAGE-EVs or/and TLR4 agonist. SP2/0 tumor-bearing mouse model was established. Healthy mice and SP2/0-tumor bearing mice were treated with SP2/0-EVs or si-RAGE-EVs. SP2/0 CM or SP2/0-EVs stimulated ROS, inflammatory responses, and myotube atrophy in C2C12 cells. GW4869 blocked EV secretion and the effects of SP2/0 CM. RAGE mRNA expression in serum EVs was increased in MM&Sarcopenia patients and RAGE knockdown in SP2/0-EVs partially nullified SP2/0-EVs' effects. SP2/0-EVs activated the TLR4/NF-κB p65 pathway by translocating RAGE. SP2/0-EVs-derived RAGE elevated ROS production, inflammation, and myotube atrophy in C2C12 cells and caused muscle loss in SP2/0 tumor-bearing mice by activating the TLR4/NF-κB p65 pathway. SP2/0-EVs partially recapitulated muscle loss in healthy mice. SP2/0-EVs-derived RAGE increased ROS production, inflammation, and myotube atrophy in MM through TLR4/NF-κB p65 pathway activation.
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