HYBID in osteoarthritis: Potential target for disease progression

Shengyuan Zheng; Senbo An; Yan Luo; Djandan Tadum Arthur Vithran; Shaoqu Yang; Bangbao Lu; Zhenhan Deng; Yusheng Li

doi:10.1016/j.biopha.2023.115043

HYBID in osteoarthritis: Potential target for disease progression

Biomed Pharmacother. 2023 Sep:165:115043. doi: 10.1016/j.biopha.2023.115043. Epub 2023 Jun 24.

Authors

Shengyuan Zheng¹, Senbo An², Yan Luo³, Djandan Tadum Arthur Vithran⁴, Shaoqu Yang³, Bangbao Lu⁵, Zhenhan Deng⁶, Yusheng Li⁷

Affiliations

¹ Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Clinical Medicine, Xiangya Medicine School, Central South University, Changsha, Hunan, China.
² Department of Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
³ Department of Clinical Medicine, Xiangya Medicine School, Central South University, Changsha, Hunan, China.
⁴ Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China.
⁵ Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: orthop_bangbaolu@csu.edu.cn.
⁶ Department of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, Guangdong, China. Electronic address: dengzhenhan@email.szu.edu.cn.
⁷ Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, Hunan, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: liyusheng@csu.edu.cn.

PMID: 37364478
DOI: 10.1016/j.biopha.2023.115043

Abstract

HYBID is a new hyaluronan-degrading enzyme and exists in various cells of the human body. Recently, HYBID was found to over-express in the osteoarthritic chondrocytes and fibroblast-like synoviocytes. According to these researches, high level of HYBID is significantly correlated with cartilage degeneration in joints and hyaluronic acid degradation in synovial fluid. In addition, HYBID can affect inflammatory cytokine secretion, cartilage and synovium fibrosis, synovial hyperplasia via multiple signaling pathways, thereby exacerbating osteoarthritis. Based on the existing research of HYBID in osteoarthritis, HYBID can break the metabolic balance of HA in joints through the degradation ability independent of HYALs/CD44 system and furthermore affect cartilage structure and mechanotransduction of chondrocytes. In particular, in addition to HYBID itself being able to trigger some signaling pathways, we believe that low-molecular-weight hyaluronan produced by excess degradation can also stimulate some disease-promoting signaling pathways by replacing high-molecular-weight hyaluronan in joints. The specific role of HYBID in osteoarthritis is gradually revealed, and the discovery of HYBID raises the new way to treat osteoarthritis. In this review, the expression and basic functions of HYBID in joints were summarized, and reveal potential role of HYBID as a key target in treatment for osteoarthritis.

Keywords: Cartilage degradation; HYBID; Hyaluronan; Inflammation; Osteoarthritis.

Publication types

Review

MeSH terms

Disease Progression
Humans
Hyaluronic Acid* / metabolism
Hyaluronoglucosaminidase / metabolism
Mechanotransduction, Cellular
Osteoarthritis* / drug therapy

Substances

Hyaluronic Acid
Hyaluronoglucosaminidase