New insights into the interplay between autophagy and cartilage degeneration in osteoarthritis

Lv, Xiaoman; Zhao, Ting; Dai, Youwu; Shi, Mingqin; Huang, Xiaoyi; Wei, Yuanyuan; Shen, Jiayan; Zhang, Xiaoyu; Xie, Zhaohu; Wang, Qi; Li, Zhaofu; Qin, Dongdong

doi:10.3389/fcell.2022.1089668

Cited by 10 publications

(2 citation statements)

References 93 publications

(108 reference statements)

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“…Other signaling cascades are also involved in the onset and development of OA, including wingless-related integration site (Wnt), adenosine monophosphate (AMP)-activated protein kinase (AMPK), mechanistic target of rapamycin kinase pathway (mTOR), hypoxiainducible factors (HIFs), transforming growth factor-beta (TGF-β) and bone morphogenetic protein (BMP) signaling pathways [25]. Moreover, OA chondrocytes undergo cell death and trigger extracellular matrix (ECM) degradation [31][32][33][34][35].…”

Section: Copper and Zinc Dyshomeostasis In Arthritismentioning

confidence: 99%

Carnosine, Zinc and Copper: A Menage a Trois in Bone and Cartilage Protection

Ciaffaglione,

Rizzarelli

2023

IJMS

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Dysregulated metal homeostasis is associated with many pathological conditions, including arthritic diseases. Osteoarthritis and rheumatoid arthritis are the two most prevalent disorders that damage the joints and lead to cartilage and bone destruction. Recent studies show that the levels of zinc (Zn) and copper (Cu) are generally altered in the serum of arthritis patients. Therefore, metal dyshomeostasis may reflect the contribution of these trace elements to the disease’s pathogenesis and manifestations, suggesting their potential for prognosis and treatment. Carnosine (Car) also emerged as a biomarker in arthritis and exerts protective and osteogenic effects in arthritic joints. Notably, its zinc(II) complex, polaprezinc, has been recently proposed as a drug-repurposing candidate for bone fracture healing. On these bases, this review article aims to provide an overview of the beneficial roles of Cu and Zn in bone and cartilage health and their potential application in tissue engineering. The effects of Car and polaprezinc in promoting cartilage and bone regeneration are also discussed. We hypothesize that polaprezinc could exchange Zn for Cu, present in the culture media, due to its higher sequestering ability towards Cu. However, future studies should unveil the potential contribution of Cu in the beneficial effects of polaprezinc.

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Section: Copper and Zinc Dyshomeostasis In Arthritismentioning

confidence: 99%

Carnosine, Zinc and Copper: A Menage a Trois in Bone and Cartilage Protection

Ciaffaglione,

Rizzarelli

2023

IJMS

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“…The pathophysiology of OA is still challenging. Recently, many researchers have focused on autophagy as one of major contributors to cartilage injury and OA development [9,10]. Autophagy is a cellular homeostasis process that regulates energy metabolism as well as the removal of damaged and dysfunctional macromolecules and organelles [11].…”

Section: Introductionmentioning

confidence: 99%

Autophagy in Osteoarthritis: A Double-Edged Sword in Cartilage Aging and Mechanical Stress Response: A Systematic Review

Lee,

Bahar,

Kim

et al. 2024

JCM

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Background: Although osteoarthritis (OA) development is epidemiologically multifactorial, a primary underlying mechanism is still under debate. Understanding the pathophysiology of OA remains challenging. Recently, experts have focused on autophagy as a contributor to OA development. Method: To better understand the pathogenesis of OA, we survey the literature on the role of autophagy and the molecular mechanisms of OA development. To identify relevant studies, we used controlled vocabulary and free text keywords to search the MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, Web of Science, and SCOPUS database. Thirty-one studies were included for data extraction and systematic review. Among these studies, twenty-five studies investigated the effects of autophagy in aging and OA chondrocytes, six studies examined the effects of autophagy in normal human chondrocytes, and only one study investigated the effects of mechanical stress-induced autophagy on the development of OA in normal chondrocytes. Results: The studies suggest that autophagy activation prevents OA by exerting cell-protective effects in normal human chondrocytes. However, in aging and osteoarthritis (OA) chondrocytes, the role of autophagy is intricate, as certain studies indicate that stimulating autophagy in these cells can have a cytotoxic effect, while others propose that it may have a protective (cytoprotective) effect against damage or degeneration. Conclusions: Mechanical stress-induced autophagy is also thought to be involved in the development of OA, but further research is required to identify the precise mechanism. Thus, autophagy contributions should be interpreted with caution in aging and the types of OA cartilage.

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