ArticleInternational journal of molecular sciences2008
Caffeine induces cell death via activation of apoptotic signal and inactivation of survival signal in human osteoblasts.
Article in International journal of molecular sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
45 citing papers in PubMed, 116 citations in OpenAlex.
- Human monocyte heat shock protein 72 responses to acute hypoxic exercise after 3 days of exercise heat acclimation.BioMed research international · 2015Trial
- Extracellular Hsp72 concentration relates to a minimum endogenous criteria during acute exercise-heat exposure.Cell stress & chaperones · 2014Trial
- Review
- Review
- Caffeine toxicity in zebrafish - Neurobehavioral changes, developmental defects, and oxidative stress: A review.Biomolecules & biomedicine · 2025Review
- Caffeine consumption as a potential risk factor of osteoporosis development among night shift workers: epidemiological evidences and hypothesis.International journal of occupational medicine and environmental health · 2025Review
- A Liposomal Strategy for Dual-Action Therapy in Sarcopenia: Co-Delivery of Caffeine and HAMA.International journal of molecular sciences · 2025Article
- Synthesis, characterization, and evaluation of the cytotoxic effects of caffeine nanoparticles on K562 cancer cell line.Medical oncology (Northwood, London, England) · 2025Article
- Review
- Deciphering per- and polyfluoroalkyl substances mode of action: comparative gene expression analysis in human liver spheroids.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Effects and regulatory mechanisms of bisphenol a on the increases apoptosis and decreases differentiation potential in mouse embryonic stem cells.Toxicology research · 2025Article
- Alveolar Bone Repair Dynamics in Rats Influenced by Coffee Ingestion: A Confocal Microscopy Analysis.Cureus · 2025Article
- Evaluating chemical effects on human neural cells through calcium imaging and deep learning.iScience · 2024Article
- Visualization strategies to aid interpretation of high-dimensional genotoxicity data.Environmental and molecular mutagenesis · 2024Article
- Caffeine regulates both osteoclast and osteoblast differentiation via the AKT, NF-κB, and MAPK pathways.Frontiers in pharmacology · 2024Article
- Synergistic Effect of Saccharin and Caffeine on Antiproliferative Activity in Human Ovarian Carcinoma Ovcar-3 Cells.International journal of molecular sciences · 2023Article
- Natural Products Targeting Hsp90 for a Concurrent Strategy in Glioblastoma and Neurodegeneration.Metabolites · 2022Review
- The association between coffee consumption and periodontitis: a cross-sectional study of a northern German population.Clinical oral investigations · 2022Article
- Does Drinking Coffee and Tea Affect Bone Metabolism in Patients with Inflammatory Bowel Diseases?Nutrients · 2021Review
- Neferine and lianzixin extracts have protective effects on undifferentiated caffeine-damaged PC12 cells.BMC complementary medicine and therapies · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caffeine consumption is a risk factor for osteoporosis, but the precise regulatory mechanisms are currently unknown. Here, we show that cell viability decreases in osteoblasts treated with caffeine in a dose-dependent manner. This cell death is attributed primarily to apoptosis and to a smaller extent, necrosis. Moreover, caffeine directly stimulates intracellular oxidative stress. Our data support caffeine-induced apoptosis in osteoblasts via a mitochondria-dependent pathway. The apoptotic biochemical changes were effectively prevented upon pretreatment with ROS scavengers, indicating that ROS plays a critical role as an upstream controller in the caffeine-induced apoptotic cascade. Additionally, p21-activated protein kinase 2 (PAK2) and c-Jun N-terminal kinase (JNK) were activated in caffeine-treated osteoblasts. Experiments further found that PAK2 activity is required for caffeine-induced JNK activation and apoptosis. Importantly, our data also show that caffeine triggers cell death via inactivation of the survival signal, including the ERK- and Akt-mediated anti-apoptotic pathways. Finally, exposure of rats to dietary water containing approximately 10-20 microM caffeine led to bone mineral density loss. These results demonstrate for the first time that caffeine triggers apoptosis in osteoblasts via activation of mitochondria-dependent cell death signaling and inactivation of the survival signal, and causes bone mineral density loss in vivo.
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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.