ArticleMolecular medicine (Cambridge, Mass.)2022
Lansoprazole-induced osteoporosis via the IP3R- and SOCE-mediated calcium signaling pathways.
Article in Molecular medicine (Cambridge, Mass.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Effects of Kang'ai injection combined with chemotherapy on immune function in advanced non-small cell lung cancer: a meta-analysis.Frontiers in pharmacology · 2026Pooled it
- A lansoprazole-like structure derived from Streptomyces metabolites: evaluation of its protective effects on hepatorenal function, antioxidant activity, and immune parameters in African catfish challenged with Staphylococcus aureus.Fish physiology and biochemistry · 2026Article
- Impact of Proton Pump Inhibitor Therapy on Bone Mineral Density: An Updated Systematic Review.Cureus · 2026Review
- The pivotal role of mitochondria in osteoporosis: From pathogenesis to future therapies.Biochemistry and biophysics reports · 2026Review
- Review
- Article
- Early cardioprotective effects of SGLT2i on hypertensive cardiac remodeling via STIM1/Orai1-dependent calcium signaling: beyond blood pressure control.Journal of bioenergetics and biomembranes · 2025Article
- Lead (Pb) Induces Osteotoxicity Through the Activation of Mutually Reinforced ER Stress and ROS in MC3T3-E1 Cells.Biological trace element research · 2025Article
- Sex-specific Association of Chronic Proton Pump Inhibitor Use With Reduced Bone Density and Quality.The Journal of clinical endocrinology and metabolism · 2025Article
- The role of calcium channels in osteoporosis and their therapeutic potential.Frontiers in endocrinology · 2024Review
- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- PPI-Induced Changes in Plasma Metabolite Levels Influence Total Hip Bone Mineral Density in a UK Cohort.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Clinical Use of Lansoprazole and the Risk of Osteoporosis: A Nationwide Cohort Study.International journal of environmental research and public health · 2022Article
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
backgroundMany clinical studies have shown a correlation between proton pump inhibitors (PPIs) and osteoporosis or fractures. The purpose of this study was to establish a murine model of chronic oral PPI administration to verify whether PPIs caused bone metabolic impairment and investigate the relevant molecular mechanism underlying the effects of PPIs on MC3T3-E1 murine osteoblasts.
methodsA lansoprazole-induced bone loss model was used to investigate the damaging effects of PPIs. In vivo, immunohistochemistry, Hematoxylin-Eosin (HE) staining, micro-CT analysis, and blood biochemical analyses were used to evaluate the effect of lansoprazole on bone injury in mice. In vitro, the effects of lansoprazole and related signaling pathways in MC3T3-E1 cells were investigated by CCK-8 assays, EdU assays, flow cytometry, laser confocal microscopy, patch clamping, reverse transcription-quantitative polymerase chain reaction and Western blotting.
resultsAfter 6 months of lansoprazole gavage in ICR mice, the micro-CT results showed that compared with that in the vehicle group, the bone mineral density (BMD) in the high-dose group was significantly decreased (P < 0.05), and the bone microarchitecture gradually degraded. Biochemical analysis of bone serum showed that blood calcium and phosphorus were both decreased (P < 0.01). We found that long-term administration of lansoprazole impaired skeletal function in mice. In vitro, we found that lansoprazole (LPZ) could cause calcium overload in MC3T3-E1 cells leading to apoptosis, and 2-APB, an inhibitor of IP3R calcium release channel and SOCE pathway, effectively blocked increase in calcium caused by LPZ, thus protecting cell viability.
conclusionsLongterm administration of LPZ induced osteoporotic symptoms in mice, and LPZ triggered calcium increases in osteoblasts in a concentration-dependent manner. Intracellular calcium ([Ca
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