ArticleInternational journal of molecular sciences2020
HIV-1-Infected Human Macrophages, by Secreting RANK-L, Contribute to Enhanced Osteoclast Recruitment.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Glycolysis inhibition in tuberculosis-driven metabolic rewiring reduces HIV-1 spread in macrophages.Life science alliance · 2026Article
- Moesin controls cell-cell fusion and osteoclast function.The Journal of cell biology · 2025Article
- Investigation of Osteoporosis in Persons Living with Human Immunodeficiency Virus: The HOST Study.Calcified tissue international · 2025Article
- Importance of trace elements in the immunometabolic health of people living with HIV/AIDS: a literature review.Molecular biology reports · 2024Review
- Analysis of risk factors and development of a nomogram-based prediction model for defective bony non-union.Heliyon · 2024Article
- Risk Factors Associated with Osteopenia/Osteoporosis in Antiretroviral Therapy Naive HIV Patients.Current HIV research · 2024Article
- Massively HIV-1-infected macrophages exhibit a severely hampered ability to differentiate into osteoclasts.Frontiers in immunology · 2023Article
- Bone Quality in Relation to HIV and Antiretroviral Drugs.Current HIV/AIDS reports · 2022Review
- Osteoporosis and HIV Infection.Calcified tissue international · 2022Review
- Cellular and molecular actors of myeloid cell fusion: podosomes and tunneling nanotubes call the tune.Cellular and molecular life sciences : CMLS · 2021Review
- Tissue remodeling by invadosomes.Faculty reviews · 2021Review
- The Role of the RANKL/RANK Axis in the Prevention and Treatment of Breast Cancer with Immune Checkpoint Inhibitors and Anti-RANKL.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
HIV-1 infection is frequently associated with low bone density, which can progress to osteoporosis leading to a high risk of fractures. Only a few mechanisms have been proposed to explain the enhanced osteolysis in the context of HIV-1 infection. As macrophages are involved in bone homeostasis and are critical host cells for HIV-1, we asked whether HIV-1-infected macrophages could participate in bone degradation. Upon infection, human macrophages acquired some osteoclast features: they became multinucleated, upregulated the osteoclast markers RhoE and β3 integrin, and organized their podosomes as ring superstructures resembling osteoclast sealing zones. However, HIV-1-infected macrophages were not fully differentiated in osteoclasts as they did not upregulate NFATc-1 transcription factor and were unable to degrade bone. Investigating whether infected macrophages participate indirectly to virus-induced osteolysis, we showed that they produce RANK-L, the key osteoclastogenic cytokine. RANK-L secreted by HIV-1-infected macrophages was not sufficient to stimulate multinucleation, but promoted the protease-dependent migration of osteoclast precursors. In conclusion, we propose that, by stimulating RANK-L secretion, HIV-1-infected macrophages contribute to create a microenvironment that favors the recruitment of osteoclasts, participating in bone disorders observed in HIV-1 infected patients.
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