ArticleNaunyn-Schmiedeberg's archives of pharmacology2017
Carboxyamidotriazole alleviates muscle atrophy in tumor-bearing mice by inhibiting NF-κB and activating SIRT1.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. 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, 16 citations in OpenAlex.
- Carboxyamidotriazole Complexed to PLGA Is Safe, Effective, and Durable in Models of Neovascular Retinal Disease.Translational vision science & technology · 2025Article
- Ursolic Acid Alleviates Cancer Cachexia and Prevents Muscle Wasting via Activating SIRT1.Cancers · 2023Article
- Inflammation: Roles in Skeletal Muscle Atrophy.Antioxidants (Basel, Switzerland) · 2022Review
- Carnosol and its analogues attenuate muscle atrophy and fat lipolysis induced by cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2021Article
- β-LAPachone is renoprotective in streptozotocin-induced diabetic mice via regulating the PI3K/Akt/mTOR signaling pathway.Iranian journal of basic medical sciences · 2021Article
- Molecular changes in transcription and metabolic pathways underlying muscle atrophy in the CuZnSOD null mouse model of sarcopenia.GeroScience · 2020Article
- Molecular Basis for the Therapeutic Effects of Exercise on Mitochondrial Defects.Frontiers in physiology · 2020Review
- Coix seed oil ameliorates cancer cachexia by counteracting muscle loss and fat lipolysis.BMC complementary and alternative medicine · 2019Article
- Carboxyamidotriazole combined with IDO1-Kyn-AhR pathway inhibitors profoundly enhances cancer immunotherapy.Journal for immunotherapy of cancer · 2019Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cachexia is a complex disorder characterized by inflammatory responses, and it is associated with poor performance status and high mortality rate of cancer patients. Carboxyamidotriazole (CAI), a noncytotoxic chemotherapy agent, shows anti-inflammatory features in the treatment of many diseases. Here, we investigated the preventive and therapeutic effects of CAI on muscle loss that occurred in mice with advanced Lewis lung carcinoma (LLC). The carcass weights of CAI-treated mice were significantly higher than that of mice in the vehicle group from Day 19 to the end of the study. The gastrocnemius and epididymal adipose tissue weights were also increased by CAI treatment. The protective mechanisms might be attributed to the following points: CAI treatment inhibited the proteolysis in muscles by decreasing expressions of muscle-specific FoxO3 transcription factor and ubiquitin E3 ligases (MuRF1 and atrogin1). Moreover, CAI restricted the NF-κB signaling, downregulated the level of TNF-α in muscle and both TNF-α and IL-6 levels in serum, directly stimulated SIRT1 activity in vitro, and increased SIRT1 content in muscle. These results indicate that CAI can alleviate muscle wasting and is a promising drug against lung cancer cachexia.
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