Identification of EGFR as an essential regulator in chondrocytes ferroptosis of osteoarthritis using bioinformatics, in vivo, and in vitro study

Sun, Hong; Peng, Guoxuan; Chen, Kunhao; Xiong, Zhilin; Zhuang, Yong; Liu, Miao; Ning, Xu; Yang, Hua; Deng, Jin

doi:10.1016/j.heliyon.2023.e19975

Cited by 6 publications

(2 citation statements)

References 64 publications

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“…Osteoarthritis (OA) acts as the most common disabling joint disease, which seriously compromises the quality of osteoarthritic cartilages. 18,19 OA is characterized by the loss of cartilage in the primary lesion. 20 Primary OA treatment approaches involve nonpharmacological interventions combined with pharmacotherapy or surgical intervention.…”

Section: Discussionmentioning

confidence: 99%

IGF2BP1 Bolsters the Chondrocytes Ferroptosis of Osteoarthritis by Targeting m6A/MMP3 Axis

Zhao,

Dong,

Yang

et al. 2024

IJGM

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Chondrocyte degeneration and senescence are characteristics of osteoarthritis (OA) and other joint degenerative diseases, and ferroptosis has been observed to regulate the development of OA. However, the role of the N 6 -methyladenosine (m 6 A) modification in OA ferroptosis remains unclear. Methods: This study performed series of assays to investigate the function of the m 6 A reader IGF2BP1 in OA ferroptosis, including m 6 A quantitative analysis, Iron (Fe 2+ ) release analysis, Malondialdehyde (MDA) measurement, lipid peroxidation (ROS) detection and Glutathione (GSH) measurement. The molecular interaction and mechanism analysis was performed by Luciferase reporter assay, mRNA stability analysis and RNA immunoprecipitation (RIP) assay. Results: These results indicate that IGF2BP1 is upregulated in IL-1β-induced chondrocytes. Functionally, IGF2BP1 silencing represses ferroptosis, including iron (Fe 2+ ) accumulation, malondialdehyde, and reactive oxygen species (ROS). Mechanistically, among the potential downstream targets, matrix metalloproteinase-3 (MMP3) was observed to harbor a significant m 6 A modified site in the 3'-UTR. IGF2BP1 combines with MMP3 through the binding of m 6 A sites, thereby enhancing MMP3 mRNA stability. Discussion: In conclusion, our findings revealed the functions and mechanisms of m 6 A regulator IGF2BP1 in OA chondrocyte's ferroptosis, providing a novel target for OA treatment.

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Section: Discussionmentioning

confidence: 99%

IGF2BP1 Bolsters the Chondrocytes Ferroptosis of Osteoarthritis by Targeting m6A/MMP3 Axis

Zhao,

Dong,

Yang

et al. 2024

IJGM

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show abstract

“…Bioinformatics and machine learning synergistically contribute to the advancement of biomedical research by providing powerful tools for data analysis, predictive modeling, and the discovery of meaningful patterns in complex biological datasets. The integration of these technologies holds great promise in unlocking new insights into diseases and improving patient outcomes [ 18 , 19 ]. This study aimed to utilize bioinformatics and machine learning techniques to identify diagnostic biomarkers associated with OA and explore their potential applications in early diagnosis and personalized treatment.…”

Section: Introductionmentioning

confidence: 99%

Identification of diagnostic biomarkers for osteoarthritis through bioinformatics and machine learning

Wang,

Li,

Lin

2024

Heliyon

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Chondrocyte Ferritinophagy as a Molecular Mechanism of Arthritis–A Narrative Review

Liu,

Song,

Gao

et al. 2024

Cell Biochem Biophys

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Identification of EGFR as an essential regulator in chondrocytes ferroptosis of osteoarthritis using bioinformatics, in vivo, and in vitro study

Cited by 6 publications

References 64 publications

IGF2BP1 Bolsters the Chondrocytes Ferroptosis of Osteoarthritis by Targeting m6A/MMP3 Axis

IGF2BP1 Bolsters the Chondrocytes Ferroptosis of Osteoarthritis by Targeting m6A/MMP3 Axis

Identification of diagnostic biomarkers for osteoarthritis through bioinformatics and machine learning

Chondrocyte Ferritinophagy as a Molecular Mechanism of Arthritis–A Narrative Review

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