Adipokine Signaling Pathways in Osteoarthritis

Zhang, Chaofan; Lin, Yunzhi; Yan, Chun Hoi; Zhang, Wenming

doi:10.3389/fbioe.2022.865370

Cited by 9 publications

(14 citation statements)

References 161 publications

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“…An in vitro cell culture study showed that leptin could activate the NF‐κB signaling pathway to induce chondrocytes to express MMP1 and MMP13 33 . NF‐κB was also shown to be a critical factor in the adiponectin‐induced expression of bone morphogenetic protein (BMP)‐2 in osteoblasts and IL‐6 in human synovial fibroblasts 17 . Our study, in vivo and in vitro results, confirmed that NF‐κB plays an important role in FABP4‐mediated OA.…”

Section: Discussionmentioning

confidence: 99%

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Fatty acid binding protein 4 (FABP4) induces chondrocyte degeneration via activation of the NF‐κb signaling pathway

Zhang,

Lin,

et al. 2023

The FASEB Journal

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The pathogenesis of osteoarthritis (OA) is still unclear. Fatty acid binding protein 4 (FABP4), a novel adipokine, has been found to play a role in OA. This study aimed to explore the role of NF‐κB in FABP4‐induced OA. In the in vivo study, four pairs of 12‐week‐old male FABP4 knockout (KO) and wild‐type (WT) mice were included. The activation of NF‐κB was assessed. In parallel, 24 6‐week‐old male C57/Bl6 mice were fed a high‐fat diet (HFD) and randomly allocated to four groups: daily oral gavage with (1) PBS solution; (2) QNZ (NF‐κB‐specific inhibitor, 1 mg/kg/d); (3) BMS309403 (FABP4‐specific inhibitor, 30 mg/kg/d); and (4) BMS309403 (30 mg/kg/d) + QNZ (1 mg/kg/d). The diet and treatment were sustained for 4 months. The knee joints were obtained to assess cartilage degradation, NF‐κB activation, and subchondral bone sclerosis. In the in vitro study, a mouse chondrogenic cell line (ATDC5) was cultured. FABP4 was supplemented to stimulate chondrocytes, and the activation of NF‐κB was investigated. In parallel, QNZ and NF‐κB‐specific siRNA were used to inhibit NF‐κB. In vivo, the FABP4 WT mice had more significant NF‐κB activation than the KO mice. Dual inhibition of FABP4 and NF‐κB alleviated knee OA in mice. FABP4 has no significant effect on the activation of the JNK signaling pathway. In vitro, FABP4 directly activated NF‐κB in chondrocytes. The use of QNZ and NF‐κB‐siRNA significantly alleviated the expression of catabolic markers of chondrocytes induced by FABP4. FABP4 induces chondrocyte degeneration by activating the NF‐κB pathway.

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Section: Discussionmentioning

confidence: 99%

“…16 The NF-κB signaling pathway is also a center of crosstalk in adipokine-mediated OA. 17 The NF-κB pathway has been shown to play both anti-and pro-oxidant roles in the context of oxidative stress. 18 Therefore, the purpose of this study was to explore the mechanism of FABP4 in cartilage degeneration and inflammation.…”

Section: Significance Statementmentioning

confidence: 99%

Fatty acid binding protein 4 (FABP4) induces chondrocyte degeneration via activation of the NF‐κb signaling pathway

Zhang,

Lin,

et al. 2023

The FASEB Journal

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“…The hypoxia-inducible factors-2α expression causes OA by promoting Fas-mediated chondrocyte apoptosis [ 261 ]. Induced by chronic excess of glucolipid metabolism, synovium secretes adipokines, such as free fatty acids, leptin, and adiponectin, which increase the expression of cartilage-degeneration-related genes in chondrocytes [ 262 , 263 ]. Reseland et al [ 264 ] reported that leptin is released upon local mechanostimulation, which might be associated with osteoblastic development in subchondral bone remodeling.…”

Section: Perspective and Outlookmentioning

confidence: 99%

Adhesive hydrogels in osteoarthritis: from design to application

et al. 2023

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Osteoarthritis (OA) is the most common type of degenerative joint disease which affects 7% of the global population and more than 500 million people worldwide. One research frontier is the development of hydrogels for OA treatment, which operate either as functional scaffolds of tissue engineering or as delivery vehicles of functional additives. Both approaches address the big challenge: establishing stable integration of such delivery systems or implants. Adhesive hydrogels provide possible solutions to this challenge. However, few studies have described the current advances in using adhesive hydrogel for OA treatment. This review summarizes the commonly used hydrogels with their adhesion mechanisms and components. Additionally, recognizing that OA is a complex disease involving different biological mechanisms, the bioactive therapeutic strategies are also presented. By presenting the adhesive hydrogels in an interdisciplinary way, including both the fields of chemistry and biology, this review will attempt to provide a comprehensive insight for designing novel bioadhesive systems for OA therapy.

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“…Osteoarthritis (OA) is mainly characterized by articular cartilage degeneration, chronic mild synovitis, and subchondral bone degeneration (Wei & Bai, 2016). At the cellular microenvironment level, various factors could cause chondrocytes to become damaged and dysfunctional, including metabolic abnormalities (Zheng et al, 2021), extracellular matrix (ECM) degradation, oxidative stress, adipokines (Wang & He, 2018; Zhang, Lin, et al, 2022), and mechanical stimulation (Wang & He, 2018). These kinds of inflammation‐associated pathological changes could be seen as associated with different inflammatory factor secreting, including interleukin (IL)‐1, cyclooxygenases (COX), prostaglandin E (PGE; Cook et al, 2018; Dinarello, 2011), matrix metalloproteinase (MMP) family, components of the NF‐κB, tumor necrosis factor (TNF) family, and so forth (Stone et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Natural anti‐inflammatory products for osteoarthritis: From molecular mechanism to drug delivery systems and clinical trials

Su,

Yu,

Wang

et al. 2023

Phytotherapy Research

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Osteoarthritis (OA) is a degenerative joint disease that affects millions globally. The present nonsteroidal anti‐inflammatory drug treatments have different side effects, leading researchers to focus on natural anti‐inflammatory products (NAIPs). To review the effectiveness and mechanisms of NAIPs in the cellular microenvironment, examining their impact on OA cell phenotype and organelles levels. Additionally, we summarize relevant research on drug delivery systems and clinical randomized controlled trials (RCTs), to promote clinical studies and explore natural product delivery options. English‐language articles were searched on PubMed using the search terms “natural products,” “OA,” and so forth. We categorized search results based on PubChem and excluded “natural products” which are mix of ingredients or compounds without the structure message. Then further review was separately conducted for molecular mechanisms, drug delivery systems, and RCTs later. At present, it cannot be considered that NAIPs can thoroughly prevent or cure OA. Further high‐quality studies on the anti‐inflammatory mechanism and drug delivery systems of NAIPs are needed, to determine the appropriate drug types and regimens for clinical application, and to explore the combined effects of different NAIPs to prevent and treat OA.

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Adipokine Signaling Pathways in Osteoarthritis

Cited by 9 publications

References 161 publications

Fatty acid binding protein 4 (FABP4) induces chondrocyte degeneration via activation of the NF‐κb signaling pathway

Fatty acid binding protein 4 (FABP4) induces chondrocyte degeneration via activation of the NF‐κb signaling pathway

Adhesive hydrogels in osteoarthritis: from design to application

Natural anti‐inflammatory products for osteoarthritis: From molecular mechanism to drug delivery systems and clinical trials

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