Role of Signal Transduction Pathways and Transcription Factors in Cartilage and Joint Diseases

DOI DOI Web Site PubMed 被引用文献3件 参考文献126件

書誌事項

公開日
2020-01-18
資源種別
journal article
権利情報
  • http://creativecommons.org/licenses/by/4.0
DOI
  • 10.20944/preprints202001.0199.v1
  • 10.3390/ijms21041340
公開者
MDPI AG

説明

<jats:p>Osteoarthritis and rheumatoid arthritis are common cartilage and joint diseases that globally affect more than 200 and 20 million people, respectively. Several transcription factors have been implicated in the onset and progression of osteoarthritis, including Runx2, C/EBP&beta;, HIF2&alpha;, Sox4, and Sox11. IL-1&beta; also leads to osteoarthritis through NF-ĸB, I&kappa;B&zeta;, and Zn2+-ZIP8-MTF1 axis. IL-1, IL-6, and TNF&alpha; play a major pathological role in rheumatoid arthritis through NF-ĸB and JAK/STAT pathways. Indeed, inhibitory reagents for IL-1, IL-6, and TNF&alpha; provide clinical benefits for rheumatoid arthritis patients. Several growth factors, such as BMP, FGF, PTHrP, and Indian hedgehog, play roles regulating chondrocyte proliferation and differentiation. Disruption and excess of these signaling cause genetic disorders in cartilage and skeletal tissues. FOP, an autosomal genetic disorder characterized by ectopic ossification, is induced by mutant ACVR1. mTOR inhibitors were found to prevent ectopic ossification by ACVR1 mutations. ACH and related diseases are autosomal genetic diseases, which manifest severe dwarfism. CNP is currently the most promising therapy for ACH. In these ways, investigation of cartilage and chondrocyte diseases at molecular and cellular levels sheds light on the development of effective therapies. Thus, identification of signaling pathways and transcription factors implicated in these diseases is important.</jats:p>

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