Mechanical stress abnormalities promote chondrocyte senescence - The pathogenesis of knee osteoarthritis

Abstract

Knee osteoarthritis (KOA) is a common chronic disease in orthopedics, which brings great pain to patients' life and spirit. Therefore, it is necessary to elucidate the pathogenesis of KOA. The pathophysiology of KOA has been linked to numerous factors, including oxidative stress, apoptosis, cellular senescence, mitochondrial dysfunction, and inflammatory factors. Cellular senescence has grown in importance as a topic of study for age-related illnesses recently. KOA has also been discovered to be closely related to human aging, a process in which chondrocyte senescence may be crucial. Numerous researches have looked at the pathogenesis of KOA from the perspectives of mechanical stress abnormalities, oxidative stress, inflammatory overexpression, and mitochondrial dysfunction. Many studies have discovered that the primary pathogenesis of KOA is inflammatory overexpression and chondrocyte death brought on by an imbalance in the joint microenvironment. And abnormal mechanical stress is the initiating cause of oxidative stress, inflammation, and mitochondrial disorders. However, few findings have been reported in the literature on the relationship between these factors, especially for mechanical stress abnormalities, and chondrocyte senescence. This time, in order to better understand the pathogenesis of KOA and identify potential connections between chondrocyte senescence and these microenvironments in KOA, as well as oxidative stress, inflammatory overexpression, and mitochondrial dysfunction microenvironmental dysfunctions, we will use chondrocyte senescence as a starting point. This will allow us to develop new therapeutic approaches for KOA.

Keywords: Chondrocyte senescence; Inflammation; Knee osteoarthritis; Mitochondrial autophagy; Oxygen free radicals; Pizeo1.