ArticleMolecular biology reports2022
Cholesterol inhibits autophagy in RANKL-induced osteoclast differentiation through activating the PI3K/AKT/mTOR signaling pathway.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Clinical Manifestations and Risk Factors of Osteoporosis in Patients with Type 2 Diabetes Mellitus.Journal of inflammation research · 2026Article
- Research on the role and mechanism of the PI3K/Akt/mTOR signalling pathway in osteoporosis.Frontiers in endocrinology · 2025Review
- Crosstalk between Lipid Metabolism and Bone Homeostasis: Exploring Intricate Signaling Relationships.Research (Washington, D.C.) · 2024Article
- Brevilin A inhibits RANKL-induced osteoclast differentiation and bone resorption.In vitro cellular & developmental biology. Animal · 2023Article
- mTOR Signaling Pathway in Bone Diseases Associated with Hyperglycemia.International journal of molecular sciences · 2023Review
- [Akt2 inhibitor promotes M2 macrophage polarization in rats with periapical inflammation by reducing miR-155-5p expression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- The Potential of Natural Compounds Regulating Autophagy in the Treatment of Osteoporosis.Journal of inflammation research · 2023Review
- Cumulative exposure to remnant cholesterol and the risk of fragility fractures: a longitudinal cohort study.Frontiers in endocrinology · 2023Article
- The role of circadian rhythm in osteoporosis; a review.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA dysregulated balance between bone formation and bone resorption controlled by osteoblast and osteoclast will lead to osteoporosis. Cholesterol (CHO) is a crucial factor leading to osteoporosis, and autophagy appears to involve it. Therefore, we aimed to study the molecular mechanism of autophagy in CHO-induced osteoclasts differentiation.
methodsNuclear factor-κ B ligand as a receptor activator was used to induce osteoclasts differentiation of murine macrophage RAW264.7 treated with CHO, PI3-kinase inhibitor (LY294002), and Rapamycin (RAPA), respectively. Western blot assay was used to detect the expression of TRAP/ACP5 and the proteins involved in autophagy and the PI3K/AKT/mTOR signaling pathway. In addition, TRAP staining, bone resorption assay, and F-actin immunofluorescence were performed to evaluate the ability of osteoclast formation. Transmission electron microscopy and immunofluorescence were also executed to observed the expression of LC3B, and autophagosome.
resultsWhen RAW264.7 was treated with 20 μg/mL CHO for 5 consecutive days, It exhibited the optimal osteoclast activity. In addition, CHO could inhibit autophagy and activate the PI3K/AKT/mTOR signaling pathway. Moreover, the effects of CHO on osteoclast differentiation and autophagy could partially be reversed by LY294002 and RAPA.
conclusionTherefore, our results demonstrated that CHO could inhibit autophagy during osteoclast differentiation by activating the PI3K/AKT/mTOR signaling pathway. These findings provided important theoretical basis for CHO in bone resorption and formation.
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