ArticleOxidative medicine and cellular longevity2021
Chronic Ethanol Consumption Induces Osteopenia via Activation of Osteoblast Necroptosis.
Article in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Neutrophil extracellular traps (NETs) and NETosis in alcohol-associated diseases: A systematic review.Alcohol, clinical & experimental research · 2025Pooled it
- Aging Exacerbates Binge Ethanol-Mediated Bone Toxicity in Mice.Alcohol, clinical & experimental research · 2026Article
- Article
- Programmed cell death in degenerative skeletal diseases: molecular crosstalk and combinatorial therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- SIAH1-Mediated Ubiquitination and Degradation of TRIB3 Modulate Osteogenic and Adipogenic Differentiation.Stem cells international · 2026Article
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 2025Review
- Different Forms of Regulated Cell Death in Type-2-Diabetes-Mellitus-Related Osteoporosis: A Focus on Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Article
- Osteoking promotes bone formation and bone defect repair through ZBP1-STAT1-PKR-MLKL-mediated necroptosis.Chinese medicine · 2024Article
- Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.Frontiers in cell and developmental biology · 2024Review
- Dexamethasone-induced mitochondrial ROS-mediated inhibition of AMPK activity facilitates osteoblast necroptosis.Toxicology research · 2023Article
- Sarcopenic Obesity in People with Alcoholic Use Disorder: Relation with Inflammation, Vascular Risk Factors and Serum Vitamin D Levels.International journal of molecular sciences · 2023Article
- Recent Therapeutic Strategies for Excessive Chondrocyte Death in Osteoarthritis: A Review.Orthopaedic surgery · 2023Review
- Crosstalk between Inflammation and Hemorrhage/Coagulation Disorders in Primary Blast Lung Injury.Biomolecules · 2023Review
- Suffruticosol A elevates osteoblast differentiation targeting BMP2-Smad/1/5/8-RUNX2 in pre-osteoblasts.BioFactors (Oxford, England) · 2023Article
- High Glucose-Induced Kidney Injury via Activation of Necroptosis in Diabetic Kidney Disease.Oxidative medicine and cellular longevity · 2023Article
- Effects of Triterpene Soyasapogenol B fromInternational journal of molecular sciences · 2022Article
- Necroptosis: A new target for prevention of osteoporosis.Frontiers in endocrinology · 2022Review
- Targeting Cell Death: Pyroptosis, Ferroptosis, Apoptosis and Necroptosis in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic high-dose alcohol consumption impairs bone remodeling, reduces bone mass, and increases the risk of osteoporosis and bone fracture. However, the mechanisms underlying alcohol-induced osteoporosis are yet to be elucidated. In this study, we showed that excess intake of ethyl alcohol (EtOH) resulted in osteopenia and osteoblast necroptosis in mice that led to necrotic lesions and reduced osteogenic differentiation in bone marrow mesenchymal stem cells (BMMSCs). We found that EtOH treatment led to the activation of the RIPK1/RIPK3/MLKL signaling, resulting in increased osteoblast necroptosis and decreased osteogenic differentiation and bone formation both in vivo and in vitro. We further discovered that excessive EtOH treatment-induced osteoblast necroptosis might partly depend on reactive oxygen species (ROS) generation; concomitantly, ROS contributed to necroptosis of osteoblasts through a positive feedback loop involving RIPK1/RIPK3. In addition, blocking of the RIPK1/RIPK3/MLKL signaling by necrostatin-1 (Nec-1), a key inhibitor of RIPK1 kinase in the necroptosis pathway, or antioxidant N-acetylcysteine (NAC), an inhibitor of ROS, could decrease the activation of osteoblast necroptosis and ameliorate alcohol-induced osteopenia both in vivo and in vitro. Collectively, we demonstrated that chronic high-dose alcohol consumption induced osteopenia via osteoblast necroptosis and revealed that RIPK1 kinase may be a therapeutic target for alcohol-induced osteopenia.
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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 OpenQuestion graph.