Transcriptional regulation of bone and joint remodeling by NFAT
Despina Sitara,
Antonios O. Aliprantis,
Despina Sitara
Department of Infectious Diseases and Immunology, Harvard School of Public Health, Boston, MA, USA.
Search for more papers by this authorAntonios O. Aliprantis
Department of Infectious Diseases and Immunology, Harvard School of Public Health, Boston, MA, USA.
Division of Rheumatology, Allergy and Immunology, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Arthritis Center, Boston, MA, USA.
Search for more papers by this authorDespina Sitara,
Antonios O. Aliprantis,
Despina Sitara
Department of Infectious Diseases and Immunology, Harvard School of Public Health, Boston, MA, USA.
Search for more papers by this authorAntonios O. Aliprantis
Department of Infectious Diseases and Immunology, Harvard School of Public Health, Boston, MA, USA.
Division of Rheumatology, Allergy and Immunology, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Arthritis Center, Boston, MA, USA.
Search for more papers by this authorAntonios O. Aliprantis
Harvard School of Public Health651 Huntington Avenue, FXB 205Boston, MA 02115, USATel.: +1 617 432 4867Fax: +1 617 432 0084e-mail: [email protected]
Abstract
Summary: Osteoporosis and arthritis are highly prevalent diseases and a significant cause of morbidity and mortality worldwide. These diseases result from aberrant tissue remodeling leading to weak, fracture-prone bones or painful, dysfunctional joints. The nuclear factor of activated T cells (NFAT) transcription factor family controls diverse biologic processes in vertebrates. Here, we review the scientific evidence that links NFAT-regulated gene transcription to bone and joint pathology. A particular emphasis is placed on the role of NFATs in bone resorption and formation by osteoclasts and osteoblasts, respectively. In addition, emerging data that connect NFATs with cartilage biology, angiogenesis, nociception, and neurogenic inflammation are explored. The goal of this article is to highlight the importance of tissue remodeling in musculoskeletal disease and situate NFAT-driven cellular responses within this context to inspire future research endeavors.
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