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Yufeng Chen

Researcher at Sun Yat-sen University

Publications -  8
Citations -  426

Yufeng Chen is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Cartilage & Medicine. The author has an hindex of 2, co-authored 6 publications receiving 52 citations.

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Global, regional prevalence, incidence and risk factors of knee osteoarthritis in population-based studies

TL;DR: The global prevalence and incidence of knee OA varied substantially between individual countries and increased with age, and these findings can be used to better assess the global health burden of knees OA.
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Relationship between body mass index and the risk of periprosthetic joint infection after primary total hip arthroplasty and total knee arthroplasty

TL;DR: The J-shaped non-linear relationship demonstrated that increased BMI was associated with an increased risk for PJI after primary THA or TKA, and patients with ASA score ≥3, lung disease and diabetes have a higher risk of PJI.
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Diagnostic and therapeutic values of PMEPA1 and its correlation with tumor immunity in pan-cancer.

TL;DR: In this article, the prostate transmembrane protein, androgen induced 1 (PMEPA1) is differentially expressed in pan-cancer and is associated with poor prognosis in many cancer types.
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CircHIPK3 prevents chondrocyte apoptosis and cartilage degradation by sponging miR‐30a‐3p and promoting PON2

TL;DR: The findings suggested that circHIPK3 regulated chondrocyte apoptosis by mitochondrial pathway, and targeting the circHipK3/miR‐30a‐3p/PON2 axis might be a potential strategy for OA treatment.
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Clock knockdown attenuated reactive oxygen species-mediated senescence of chondrocytes through restoring autophagic flux.

TL;DR: In this paper, the authors investigated the potential role and mechanism of the circadian gene Clock in osteoarthritis (OA) pathology and found that Clock knockdown elevated antioxidant enzyme activities, diminished reactive oxygen species (ROS) production and attenuated senescence of chondrocytes via restoring autophagic flux.