Transcriptional regulation of bone and joint remodeling by NFAT
Identifieur interne : 007509 ( Istex/Corpus ); précédent : 007508; suivant : 007510Transcriptional regulation of bone and joint remodeling by NFAT
Auteurs : Despina Sitara ; Antonios O. AliprantisSource :
- Immunological Reviews [ 0105-2896 ] ; 2010-01.
English descriptors
- KwdEn :
- Acad, Aliprantis, Alkaline phosphatase, Angiogenesis, Anion exchanger, Arthritis, Arthritis rheum, Articular, Articular cartilage, Better understanding, Biochem, Biochem biophys, Biol, Biol chem, Biologic processes, Bone formation, Bone loss, Bone mass, Bone resorption, Bone surface, Calcineurin, Calcineurin inhibitors, Calcineurin nfat axis, Calcineurin nfat pathway, Calcineurin nfats, Cartilage, Cartilage biology, Catabolic, Catabolic enzymes, Catabolic pathways, Chem, Cherubism, Chondrocyte, Chondrocyte proliferation, Chondrocytes, Cytokine, Degradative enzymes, Differentiation, Endothelial, Endothelial cells, Exchanger, Further experimentation, Gene, Gene expression, Genes encoding, Goldring, Growth factor, Hco3, Higher levels, Immune, Immune system, Immunol, John wiley sons, Knockout, Knockout mice, Ligand, Macrophage, Mast cells, Master regulator, Mouse, Mutation, Neuron, Neuropeptides, Nfat, Nfat activation, Nfat family members, Nfat pathway, Nfat proteins, Nfatc1, Nfatc1 expression, Nfatc2, Nfats, Nuclear factor, Nuclear translocation, Osteoarthritis, Osteoblast, Osteoblast differentiation, Osteoclast, Osteoclast differentiation, Osteoclast formation, Osteoclast precursors, Osteoclastogenesis, Osteopetrosis, Osteoporosis, Pathogenesis, Pathway, Peptide, Periarticular, Periarticular bone, Pharmacologic, Pharmacologic inhibition, Phenotype, Phosphatase, Precursor, Proc natl acad, Promoter, Rankl, Receptor, Regulator, Regulatory domain, Resorption, Resorption lacuna, Reviews sitara aliprantis bone, Rheum, Rheumatoid, Rheumatoid arthritis, Sitara, Sitara aliprantis bone, Synovial, Synovial angiogenesis, Synoviocytes, Synovium, Takayanagi, Tnfa, Transcription, Transcription factor, Transcriptional, Vegf, Vegf pathway, Vertebrate, Vertebrate body plan, Wildtype, Wildtype mice.
- Teeft :
- Acad, Aliprantis, Alkaline phosphatase, Angiogenesis, Anion exchanger, Arthritis, Arthritis rheum, Articular, Articular cartilage, Better understanding, Biochem, Biochem biophys, Biol, Biol chem, Biologic processes, Bone formation, Bone loss, Bone mass, Bone resorption, Bone surface, Calcineurin, Calcineurin inhibitors, Calcineurin nfat axis, Calcineurin nfat pathway, Calcineurin nfats, Cartilage, Cartilage biology, Catabolic, Catabolic enzymes, Catabolic pathways, Chem, Cherubism, Chondrocyte, Chondrocyte proliferation, Chondrocytes, Cytokine, Degradative enzymes, Differentiation, Endothelial, Endothelial cells, Exchanger, Further experimentation, Gene, Gene expression, Genes encoding, Goldring, Growth factor, Hco3, Higher levels, Immune, Immune system, Immunol, John wiley sons, Knockout, Knockout mice, Ligand, Macrophage, Mast cells, Master regulator, Mouse, Mutation, Neuron, Neuropeptides, Nfat, Nfat activation, Nfat family members, Nfat pathway, Nfat proteins, Nfatc1, Nfatc1 expression, Nfatc2, Nfats, Nuclear factor, Nuclear translocation, Osteoarthritis, Osteoblast, Osteoblast differentiation, Osteoclast, Osteoclast differentiation, Osteoclast formation, Osteoclast precursors, Osteoclastogenesis, Osteopetrosis, Osteoporosis, Pathogenesis, Pathway, Peptide, Periarticular, Periarticular bone, Pharmacologic, Pharmacologic inhibition, Phenotype, Phosphatase, Precursor, Proc natl acad, Promoter, Rankl, Receptor, Regulator, Regulatory domain, Resorption, Resorption lacuna, Reviews sitara aliprantis bone, Rheum, Rheumatoid, Rheumatoid arthritis, Sitara, Sitara aliprantis bone, Synovial, Synovial angiogenesis, Synoviocytes, Synovium, Takayanagi, Tnfa, Transcription, Transcription factor, Transcriptional, Vegf, Vegf pathway, Vertebrate, Vertebrate body plan, Wildtype, Wildtype mice.
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.
Url:
DOI: 10.1111/j.0105-2896.2009.00849.x
Links to Exploration step
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<front><div type="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.</div>
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<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.</abstract>
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