Open Access

REVIEW

Regulatory role of NFAT1 signaling in articular chondrocyte activities and osteoarthritis pathogenesis

MINGCAI ZHANG, TANNER CAMPBELL, SPENCER FALCON, JINXI WANG^*

Harrington Laboratory for Molecular Orthopedics, Department of Orthopedic Surgery, University of Kansas Medical Center, Kansas City, USA

* Corresponding Author: JINXI WANG. Email:

BIOCELL 2023, 47(10), 2125-2132. https://doi.org/10.32604/biocell.2023.030161

Received 24 March 2023; Accepted 26 July 2023; Issue published 08 November 2023

Abstract

Osteoarthritis (OA), the most common form of joint disease, is characterized clinically by joint pain, stiffness, and deformity. OA is now considered a whole joint disease; however, the breakdown of the articular cartilage remains the major hallmark of the disease. Current treatments targeting OA symptoms have a limited impact on impeding or reversing the OA progression. Understanding the molecular and cellular mechanisms underlying OA development is a critical barrier to progress in OA therapy. Recent studies by the current authors’ group and others have revealed that the nuclear factor of activated T cell 1 (NFAT1), a member of the NFAT family of transcription factors, regulates the expression of many anabolic and catabolic genes in articular chondrocytes of adult mice. Mice lacking NFAT1 exhibit normal skeletal development but display OA in both appendicular and spinal facet joints as adults. This review mainly focuses on the recent advances in the regulatory role of NFAT1 transcription factor in the activities of articular chondrocytes and its implication in the pathogenesis of OA.

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