Fisetin suppresses chondrocyte senescence and attenuates osteoarthritis progression by targeting SIRT6 DOI Creative Commons
Xuezhong Wang, Xuyang Li, Jianlin Zhou

и другие.

Research Square (Research Square), Год журнала: 2023, Номер unknown

Опубликована: Ноя. 20, 2023

Abstract Background Osteoarthritis (OA), the most common type of arthritis, is a highly prevalent age-related joint disease particularly in subjects over 65 years old. The chronic rise senescent cells closely correlates with diseases including OA, and senescence-associated secretory phenotype (SASP) implicated pathogenesis OA cartilage degeneration. Sirtuin 6 (SIRT6) probable to be key senescence-related regulator. Fisetin (FST), natural flavonol flavonoid family, recommended senolytic that extends health lifespan. However, potential chondroprotective effects FST on rats remain largely unclarified. This study aimed investigate ameliorative relationship SIRT6, detailed mechanisms from both anti-inflammatory anti-senescent perspectives. Methods Rats were subjected destabilization medial meniscus (DMM) surgery induce experimental model vivo. Chondrocytes treated IL-1β utilized mimic cell vitro. Intra-articular injection FST, OSS_128167 (OSS, SIRT6 inhibitor), MDL800 (MDL, agonist) vivo or incubation IL-1β-induced rat chondrocytes vitro performed determine link SIRT6. Results level was negatively correlated severity. downregulation validated cartilages DMM IL-1β-treated chondrocytes. Of note, We demonstrated could activate Both administration activation using MDL rescued erosion, decreased extracellular matrix (ECM) degradation, prevented apoptosis, improved detrimental phenotype. alleviative against inflammation, ECM senescence also confirmed IL-1β-stimulated Conclusion loss occurs articular which linked aging. attenuates injury-induced aging-related changes by targeting

Язык: Английский

Fisetin suppresses chondrocyte senescence and attenuates osteoarthritis progression by targeting sirtuin 6 DOI
Xuezhong Wang, Xuyang Li, Jianlin Zhou

и другие.

Chemico-Biological Interactions, Год журнала: 2024, Номер 390, С. 110890 - 110890

Опубликована: Янв. 24, 2024

Язык: Английский

Процитировано

11
Current advances in animal model of meniscal injury: From meniscal injury to osteoarthritis DOI Creative Commons
X. Peng,

Fashuai Wu,

Yuxiang Hu

и другие.

Journal of Orthopaedic Translation, Год журнала: 2025, Номер 50, С. 388 - 402

Опубликована: Янв. 1, 2025

Meniscal injury is a prevalent orthopedic practice that causes articular cartilage wear and degeneration due to tissue damage or loss, may eventually result in the occurrence of knee osteoarthritis (KOA). Hence, investigating structural regeneration mechanical function restoration meniscus after pivotal research topic for preventing KOA. Animal models are essential therapeutic strategies meniscal injuries their clinical translation, yet no current model can fully recapitulate complexity human injuries. This review aims categorize animal by establishment methods, elucidate principles procedures, discuss suitability limitations each model. We delineate pros cons different simulating pathology biomechanics injury. also analyze species regarding structure, function, repair potential, implications selection. conclude selecting an appropriate requires comprehensive consideration various factors, such as aims, anticipated outcomes, feasibility. Furthermore, translate novel approaches applications more safely effectively, future development should emphasize aspects choosing animals suitable age. The Translational Potential this Article: methods provides overview routinely employed experimental facilitate translation OA-related research.

Язык: Английский

Процитировано

1
Signalling interaction between β‐catenin and other signalling molecules during osteoarthritis development DOI Creative Commons
Jing Feng, Qing Zhang, Feifei Pu

и другие.

Cell Proliferation, Год журнала: 2024, Номер 57(6)

Опубликована: Янв. 10, 2024

Abstract Osteoarthritis (OA) is the most prevalent disorder of synovial joint affecting multiple joints. In past decade, we have witnessed conceptual switch OA pathogenesis from a ‘wear and tear’ disease to entire joint. Extensive studies been conducted understand underlying mechanisms using genetic mouse models ex vivo tissues derived individuals with OA. These revealed that signalling pathways are involved in development, including canonical Wnt/β‐catenin its interaction other pathways, such as transforming growth factor β (TGF‐β), bone morphogenic protein (BMP), Indian Hedgehog (Ihh), nuclear κB (NF‐κB), fibroblast (FGF), Notch. The identification currently underway specific molecule(s) key pathway(s) playing decisive role development need be evaluated. This review will focus on recent progresses understanding critical β‐catenin TGF‐β, BMP, Notch, Ihh, NF‐κB, FGF. Understanding these novel insights into integration complex gene regulatory network during help us identify pathway leading discovery therapeutic strategies for intervention.

Язык: Английский

Процитировано

7
The phytochemistry, pharmacology, pharmacokinetics, quality control, and toxicity of Forsythiae Fructus: An updated systematic review DOI
Jinjin Li, Zihao Chen, Chengjun Liu

и другие.

Phytochemistry, Год журнала: 2024, Номер 222, С. 114096 - 114096

Опубликована: Апрель 17, 2024

Язык: Английский

Процитировано

7
Ubiquitination and deubiquitination: Implications for the pathogenesis and treatment of osteoarthritis DOI Creative Commons

Shibo Su,

Ruijiao Tian,

Yang Jiao

и другие.

Journal of Orthopaedic Translation, Год журнала: 2024, Номер 49, С. 156 - 166

Опубликована: Окт. 11, 2024

Язык: Английский

Процитировано

6
The Multifaceted Protective Role of Nuclear Factor Erythroid 2-Related Factor 2 in Osteoarthritis: Regulation of Oxidative Stress and Inflammation DOI Creative Commons
Weibei Sheng, Yaohang Yue, Tiantian Qi

и другие.

Journal of Inflammation Research, Год журнала: 2024, Номер Volume 17, С. 6619 - 6633

Опубликована: Сен. 1, 2024

Osteoarthritis (OA) is a chronic degenerative joint disease characterized by the degradation of cartilage, subchondral bone sclerosis, synovitis, and structural changes in joint. Recent research has highlighted role various genes pathogenesis progression OA, with nuclear factor erythroid 2-related 2 (NRF2) emerging as critical player. NRF2, vital transcription factor, plays key regulating OA microenvironment slowing disease's progression. It modulates expression several antioxidant enzymes, such Heme oxygenase-1 (HO-1) NAD(P)H oxidoreductase 1 (NQO1), among others, which help reduce oxidative stress. Furthermore, NRF2 inhibits kappa-B (NF-κB) signaling pathway, thereby decreasing inflammation, pain, breakdown cartilage extracellular matrix, while also mitigating cell aging death. This review discusses NRF2's impact on stress, aging, death modes (such apoptosis, necroptosis, ferroptosis) OA-affected chondrocytes. The macrophages, synovial fibroblasts was discussed. covers preserving matrix alleviating pain. purpose this to provide comprehensive understanding protective mechanisms highlighting its potential therapeutic target underscoring significance development novel treatment strategies for OA.

Язык: Английский

Процитировано

4
MiR-455-5p Mitigates Interleukin-1 β-induced Chondrocyte Damage Linked to Osteoarthritis by Targeting TNFAIP8 DOI Creative Commons
Tao Zhang, Wei Wang, Jinlei Sun

и другие.

Journal of physiological investigation., Год журнала: 2025, Номер unknown

Опубликована: Март 31, 2025

MicroRNAs have been extensively implicated in osteoarthritis (OA) progression. Our study aims to investigate the impact of miR-455-5p on OA progression and related molecular mechanisms. Cartilage tissues were collected from patients with femoral neck fractures. An vitro model was established by inducing injury human chondrocytes (CHON-001) interleukin (IL)-1 β. Cell viability apoptosis measured cell counting kit-8 flow cytometry assays, respectively. enzyme-linked immunosorbent assay performed measure concentrations inflammation factors, oxidative stress evaluated detecting superoxide dismutase activity malondialdehyde levels. TargetScan used predict binding sites between tumor necrosis factor (TNF)-α-induced protein 8 (TNFAIP8), which then confirmed dual-luciferase reporter assays. Quantitative real-time polymerase chain reaction western blot analysis employed markers. initial observations showed that expression downregulated cartilage IL-1 β-treated CHON-001 cells compared normal untreated cells. Overexpression significantly protected β-induced recovering viability, inhibiting inflammation, apoptosis, stress. TNFAIP8 targeted negatively regulated miR-455-5p. knockdown imitated, while overexpression reversed effects mediated chondrocyte injury, as further levels iNOS, cleaved caspase-3, NQO1, Col2a1, MMP13. Collectively, these results suggest may serve a new therapeutic target for targeting alleviate injury.

Язык: Английский

Процитировано

0
Curcumenol regulates Histone H3K27me3 demethylases KDM6B affecting Succinic acid metabolism to alleviate cartilage degeneration in knee osteoarthritis DOI

Weijian Chen,

Jiacong Xiao,

Yi Zhou

и другие.

Phytomedicine, Год журнала: 2024, Номер 133, С. 155922 - 155922

Опубликована: Авг. 3, 2024

Язык: Английский

Процитировано

3
NOX1-mediated oxidative stress induces chondrocyte ferroptosis by inhibiting the Nrf2/HO-1 pathway DOI Creative Commons

Lin Tao,

Keda Yang, Ke Wang

и другие.

Scientific Reports, Год журнала: 2024, Номер 14(1)

Опубликована: Авг. 27, 2024

Osteoarthritis (OA) is a common joint disease associated with the aging of population, and it reduces quality life patients. It characterized by destruction articular cartilage secretion inflammatory cytokines. Owing to unclear pathogenesis OA, current treatment methods have significant limitations. Oxidative stress has been revealed play an important role in development OA. Our experiments indicated that levels GSH decreased level MDA increased chondrocytes, which induced ferroptosis chondrocytes We also was main mechanism caused addition activator erastin inhibitor ferrostatin-1. NOX1 modulator oxidative increasing generation reactive species (ROS). suppressed expression through cell transfection. The collagen II MMP13, IL-1β TNF-α were reversed. An increase mitochondrial membrane potential decrease intracellular ROS indicate improvement damage. Additionally, we determined effect Nrf2/HO-1 pathway on NOX1-mediated chondrocyte injury. found inhibited Nrf2/HO-1, but activation Nrf2 improved damage vivo vitro. This study induces inhibiting pathway. findings contribute revealing providing targets for drug design optimizing clinical

Язык: Английский

Процитировано

3
Anti-Osteoarthritis Mechanism of the Nrf2 Signaling Pathway DOI Creative Commons
Sarmistha Saha, Nazih Y. Rebouh

Biomedicines, Год журнала: 2023, Номер 11(12), С. 3176 - 3176

Опубликована: Ноя. 29, 2023

Osteoarthritis (OA) is a chronic degenerative disease and the primary pathogenic consequence of OA inflammation, which can affect variety tissues including synovial membrane, articular cartilage, subchondral bone. The development intra-articular microenvironment be significantly influenced by shift macrophages between pro-inflammatory anti-inflammatory phenotypes. By regulating macrophage inflammatory responses, NF-κB signaling route essential in therapy OA; whereas, nuclear factor erythroid 2-related 2 (Nrf2) pathway appears to manage relationship oxidative stress inflammation. Additionally, it has been demonstrated that under there significant interaction transcriptional pathways involving Nrf2 NF-κB. Studying how affects inflammation cellular metabolism may help us understand treat reprogramming behavior because thought metabolism. candidates for treating promoting an mechanism activating are also reviewed this paper.

Язык: Английский

Процитировано

8