Mechanisms of tissue degeneration mediated by periostin in spinal degenerative diseases and their implications for pathology and diagnosis: a review.

biomarker bone metabolic diseases inflammation mechanical stress pathway periostin spinal degenerative diseases

Journal

Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047

Informations de publication

Date de publication:
2023
Historique:
received: 13 08 2023
accepted: 18 09 2023
medline: 29 11 2023
pubmed: 29 11 2023
entrez: 29 11 2023
Statut: epublish

Résumé

Periostin (POSTN) serves a dual role as both a matricellular protein and an extracellular matrix (ECM) protein and is widely expressed in various tissues and cells. As an ECM protein, POSTN binds to integrin receptors, transduces signals to cells, enabling cell activation. POSTN has been linked with various diseases, including atopic dermatitis, asthma, and the progression of multiple cancers. Recently, its association with orthopedic diseases, such as osteoporosis, osteoarthritis resulting from cartilage destruction, degenerative diseases of the intervertebral disks, and ligament degenerative diseases, has also become apparent. Furthermore, POSTN has been shown to be a valuable biomarker for understanding the pathophysiology of orthopedic diseases. In addition to serum POSTN, synovial fluid POSTN in joints has been reported to be useful as a biomarker. Risk factors for spinal degenerative diseases include aging, mechanical stress, trauma, genetic predisposition, obesity, and metabolic syndrome, but the cause of spinal degenerative diseases (SDDs) remains unclear. Studies on the pathophysiological effects of POSTN may significantly contribute toward the diagnosis and treatment of spinal degenerative diseases. Therefore, in this review, we aim to examine the mechanisms of tissue degeneration caused by mechanical and inflammatory stresses in the bones, cartilage, intervertebral disks, and ligaments, which are crucial components of the spine, with a focus on POSTN.

Identifiants

pubmed: 38020106
doi: 10.3389/fmed.2023.1276900
pmc: PMC10645150
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

1276900

Informations de copyright

Copyright © 2023 Yoshihara, Morimoto, Hirata, Murayama, Nonaka, Tsukamoto, Toda, Kobayashi, Izuhara and Mawatari.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Tomohito Yoshihara (T)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Tadatsugu Morimoto (T)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Hirohito Hirata (H)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Masatoshi Murayama (M)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Toshihiro Nonaka (T)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Masatsugu Tsukamoto (M)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Yu Toda (Y)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Takaomi Kobayashi (T)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Kenji Izuhara (K)

Division of Medical Biochemistry, Department of Biomolecular Sciences, Saga Medical School, Saga, Japan.

Masaaki Mawatari (M)

Department of Orthopaedic Surgery, Faculty of Medicine, Saga University, Saga, Japan.

Classifications MeSH