Kelesidis Theodoros, Currier Judith S, Yang Otto O, Brown Todd T
Department of Medicine, Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Department of Medicine, Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
AIDS Rev. 2014 Jul-Sep;16(3):123-33.
Patients with HIV‑1 infection often develop multiple complications and comorbidities, including osteoporosis and atherosclerosis. The receptor activator of nuclear factor kappa-B/receptor activator of nuclear factor kappa-B ligand/osteoprotegerin axis has been identified as a possible common link between osteoporosis and vascular diseases. Since the discovery of this axis, much has been learned about its role in controlling skeletal biology and less about its role in the context of vascular biology. However, the exact role of the receptor activator of nuclear factor kappa-B ligand/osteoprotegerin axis in HIV infection is not completely understood. In this review we examine the mechanisms by which inflammation and immune dysregulation in HIV‑1 infection may impact bone turnover and atherogenesis through perturbations in the receptor activator of nuclear factor kappa-B/receptor activator of nuclear factor kappa-B ligand/osteoprotegerin axis.
HIV-1感染患者常出现多种并发症和合并症,包括骨质疏松和动脉粥样硬化。核因子κB受体激活剂/核因子κB配体受体激活剂/骨保护素轴已被确定为骨质疏松与血管疾病之间可能的共同联系。自该轴被发现以来,人们对其在控制骨骼生物学中的作用了解很多,而对其在血管生物学背景下的作用了解较少。然而,核因子κB配体受体激活剂/骨保护素轴在HIV感染中的确切作用尚未完全明确。在本综述中,我们探讨了HIV-1感染中的炎症和免疫失调可能通过干扰核因子κB受体激活剂/核因子κB配体受体激活剂/骨保护素轴来影响骨转换和动脉粥样硬化发生的机制。