ArticleAlcohol and alcoholism (Oxford, Oxfordshire)2017
Alcohol Induces Cellular Senescence and Impairs Osteogenic Potential in Bone Marrow-Derived Mesenchymal Stem Cells.
Article in Alcohol and alcoholism (Oxford, Oxfordshire), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 2 of them syntheses that pooled it.
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
37 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Pooled it
- Alcohol intake and the risk of osteonecrosis of the femoral head in Japanese populations: a dose-response meta-analysis of case-control studies.Clinical rheumatology · 2017Pooled it
- Effects of resveratrol on bone health in type 2 diabetic patients. A double-blind randomized-controlled trial.Nutrition & diabetes · 2018Trial
- Mesenchymal stromal/stem cells in tumour initiation, progression and therapy.Nature reviews. Cancer · 2026Review
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Hepatic osteodystrophy: An underrecognized metabolic bone disease.World journal of hepatology · 2025Review
- The Role of Senolytics in Osteoporosis.Biomolecules · 2025Review
- Predicting iliac bone marrow harvest success in osteonecrosis of femoral head using preoperative bone scintigraphy uptake: a cross sectional study.BMC musculoskeletal disorders · 2025Article
- Cross-talk of inflammation and cellular senescence: a new insight into the occurrence and progression of osteoarthritis.Bone research · 2024Review
- Emerging role of liver-bone axis in osteoporosis.Journal of orthopaedic translation · 2024Review
- Linking alcohol use to Alzheimer's disease: Interactions with aging and APOE along immune pathways.Medical research archives · 2024Article
- The association of alcohol use disorder with revision rates and post-operative complications in total shoulder arthroplasty.Shoulder & elbow · 2024Article
- Osteopontin Rejuvenates Senescent Adipose-Derived Stem Cells and Restores their Bone Tissue Regenerative Function.Stem cell reviews and reports · 2024Article
- Musculoskeletal and Psychological Rehabilitation.Indian journal of orthopaedics · 2023Review
- Article
- Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Exercise improved bone health in aging mice: a role of SIRT1 in regulating autophagy and osteogenic differentiation of BMSCs.Frontiers in endocrinology · 2023Article
- Targeting ferroptosis, a novel programmed cell death, for the potential of alcohol-related liver disease therapy.Frontiers in pharmacology · 2023Review
- [Progress of pathogenesis and genetics of alcohol-induced osteonecrosis of femoral head].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2022Review
- Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review.Cells · 2022Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsChronic and excessive alcohol consumption is a high-risk factor for osteoporosis. Bone marrow-derived mesenchymal stem cells (BM-MSCs) play an important role in bone formation; however, they are vulnerable to ethanol (EtOH). The purpose of this research was to investigate whether EtOH could induce premature senescence in BM-MSCs and subsequently impair their osteogenic potential.
methodsHuman BM-MSCs were exposed to EtOH ranging from 10 to 250 mM. Senescence-associated β-galactosidase (SA-β-gal) activity, cell cycle distribution, cell proliferation and reactive oxygen species (ROS) were evaluated. Mineralization and osteoblast-specific gene expression were evaluated during osteogenesis in EtOH-treated BM-MSCs. To investigate the role of silent information regulator Type 1 (SIRT1) in EtOH-induced senescence, resveratrol (ResV) was used to activate SIRT1 in EtOH-treated BM-MSCs.
resultsEtOH treatments resulted in senescence-associated phenotypes in BM-MSCs, such as decreased cell proliferation, increased SA-β-gal activity and G0/G1 cell cycle arrest. EtOH also increased the intracellular ROS and the expression of senescence-related genes, such as p16INK4α and p21. The down-regulated levels of SIRT1 accompanied with suppressed osteogenic differentiation were confirmed in EtOH-treated BM-MSCs. Activation of SIRT1 by ResV partially counteracted the effects of EtOH by decreasing senescence markers and rescuing the inhibited osteogenesis.
conclusionEtOH treatments induced premature senescence in BM-MSCs in a dose-dependent manner that was responsible for EtOH-impaired osteogenic differentiation. Activation of SIRT1 was effective in ameliorating EtOH-induced senescence phenotypes in BMSCs and could potentially lead to a new strategy for clinically preventing or treating alcohol-induced osteoporosis. SHORT SUMMARY: Ethanol (EtOH) treatments induce premature senescence in marrow-derived mesenchymal stem cells in a dose-dependent manner that is responsible for EtOH-impaired osteogenic differentiation. Activation of SIRT1 is effective in ameliorating EtOH-induced senescence phenotypes, which potentially leads to a new strategy for clinically treating alcohol-induced osteoporosis.
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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.