ArticleeLife2024
Chemotherapy activates inflammasomes to cause inflammation-associated bone loss.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 5 citations in OpenAlex.
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- Tumor survivors' musculoskeletal health assessment: advances in imaging biomarkers for cancer treatment-related sequelae.Journal of orthopaedic surgery and research · 2026Review
- Juvenile Doxorubicin Exposure Causes Lasting Trabecular Bone Loss in Mice: A Preclinical Model of Long-Term Skeletal Damage.Cancers · 2026Article
- Comparative phenotypic and molecular profiling of replicative and chemically-induced senescence in articular chondrocytes.Cell death discovery · 2026Article
- Doxorubicin induces bone loss and modifies multiple cell populationsJournal of bone oncology · 2026Article
- IL-1 signaling and inflammasomes in acute myeloid leukemia: mechanisms and therapeutic opportunities.Cellular and molecular life sciences : CMLS · 2025Review
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- Mechanistic insights into chemotherapy-induced circadian disruption using rodent models.Trends in neurosciences · 2025Review
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- Bone-protective effects of deer-hide gelatin in cyclophosphamide-induced osteoporosis rats.Frontiers in pharmacology · 2025Article
- Tadalafil pretreatment attenuates doxorubicin-induced hepatorenal toxicity by modulating oxidative stress and inflammation in Wistar rats.Toxicology reports · 2024Article
- The Role of Inflammasome-Associated Innate Immune Receptors in Cancer.Immune network · 2024Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Chemotherapy is a widely used treatment for a variety of solid and hematological malignancies. Despite its success in improving the survival rate of cancer patients, chemotherapy causes significant toxicity to multiple organs, including the skeleton, but the underlying mechanisms have yet to be elucidated. Using tumor-free mouse models, which are commonly used to assess direct off-target effects of anti-neoplastic therapies, we found that doxorubicin caused massive bone loss in wild-type mice, a phenotype associated with increased number of osteoclasts, leukopenia, elevated serum levels of danger-associated molecular patterns (DAMPs; e.g. cell-free DNA and ATP) and cytokines (e.g. IL-1β and IL-18). Accordingly, doxorubicin activated the absent in melanoma (AIM2) and NLR family pyrin domain containing 3 (NLRP3) inflammasomes in macrophages and neutrophils, causing inflammatory cell death pyroptosis and NETosis, which correlated with its leukopenic effects. Moreover, the effects of this chemotherapeutic agent on cytokine secretion, cell demise, and bone loss were attenuated to various extent in conditions of AIM2 and/or NLRP3 insufficiency. Thus, we found that inflammasomes are key players in bone loss caused by doxorubicin, a finding that may inspire the development of a tailored adjuvant therapy that preserves the quality of this tissue in patients treated with this class of drugs.
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Registered trials
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.