Transcriptional regulation of bone and joint remodeling by NFAT

Despina Sitara, Antonios O. Aliprantis

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)286-300
Number of pages15
JournalImmunological Reviews
Volume233
Issue number1
DOIs
StatePublished - Jan 2010

Fingerprint

NFATC Transcription Factors
Bone Remodeling
Joints
Neurogenic Inflammation
Musculoskeletal Diseases
TCF Transcription Factors
Choristoma
Nociception
Bone Fractures
Osteoclasts
Bone Resorption
Osteoblasts
Osteogenesis
Osteoporosis
Arthritis
Cartilage
Vertebrates
Transcription Factors
Pathology
Morbidity

Keywords

  • NFAT
  • Osteoarthritis
  • Osteoblast
  • Osteoclast
  • Osteoporosis
  • Rheumatoid arthritis

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Transcriptional regulation of bone and joint remodeling by NFAT. / Sitara, Despina; Aliprantis, Antonios O.

In: Immunological Reviews, Vol. 233, No. 1, 01.2010, p. 286-300.

Research output: Contribution to journalArticle

Sitara, Despina ; Aliprantis, Antonios O. / Transcriptional regulation of bone and joint remodeling by NFAT. In: Immunological Reviews. 2010 ; Vol. 233, No. 1. pp. 286-300.
@article{f3eed5b0e11a41069b4b0c0ebe7688d3,
title = "Transcriptional regulation of bone and joint remodeling by NFAT",
abstract = "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.",
keywords = "NFAT, Osteoarthritis, Osteoblast, Osteoclast, Osteoporosis, Rheumatoid arthritis",
author = "Despina Sitara and Aliprantis, {Antonios O.}",
year = "2010",
month = "1",
doi = "10.1111/j.0105-2896.2009.00849.x",
language = "English (US)",
volume = "233",
pages = "286--300",
journal = "Immunological Reviews",
issn = "0105-2896",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Transcriptional regulation of bone and joint remodeling by NFAT

AU - Sitara, Despina

AU - Aliprantis, Antonios O.

PY - 2010/1

Y1 - 2010/1

N2 - 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.

AB - 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.

KW - NFAT

KW - Osteoarthritis

KW - Osteoblast

KW - Osteoclast

KW - Osteoporosis

KW - Rheumatoid arthritis

UR - http://www.scopus.com/inward/record.url?scp=73249128394&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=73249128394&partnerID=8YFLogxK

U2 - 10.1111/j.0105-2896.2009.00849.x

DO - 10.1111/j.0105-2896.2009.00849.x

M3 - Article

VL - 233

SP - 286

EP - 300

JO - Immunological Reviews

JF - Immunological Reviews

SN - 0105-2896

IS - 1

ER -