Role of adiponectin in osteoarthritis

Abstract

Osteoarthritis (OA) is a widespread and most common joint disease which leads to social cost increasing accompany with aging population. Surgery is often the final treatment option. The major progression of OA includes cartilage degradation caused by chondrocytes metabolism imbalance. So, the molecular mechanisms of action in chondrocytes may provide insights into treatment methods for OA. Adiponectin is an adipokine with many biological functions in the cell metabolism. Numerous studies have illustrated that adiponectin has diverse biological effects, such as inhibition of cell apoptosis. It regulates various functions in different organs, including muscle, adipose tissue, brain, and bone, and regulates skeletal homeostasis. However, the relationship between adiponectin and cell death in the progression of OA needs further investigation. We elaborate the structure and function and the effect of adiponectin and state the correlation and intersection between adiponectin, autophagy, inflammation, and OA. From the perspective of oxidative stress, apoptosis, pyroptosis, and autophagy, we discuss the possible association between adiponectin, chondrocyte metabolism, and inflammatory factor efforts in OA. What’s more, we summarize the possible treatment methods, including the use of adiponectin as a drug target, and highlight the potential future mechanistic research. In this review, we summarize the molecular pathways and mechanisms of action of adiponectin in chondrocyte inflammation and death and the pathogenesis of OA. We also review the research on adiponectin as a target for treating OA. These studies provide a novel perspective to explore more effective treatment options considering the complex interrelationship between inflammation and metabolism in OA.

Articular Cartilage Regeneration via Induced Chondrocyte Autophagy by Sustained Release of Leptin Inhibitor from Thermo‐Sensitive Hydrogel through STAT3/REDD1/mTORC1 Cascade

“…[4] Several studies have established a correlation between adipokines released by adipose tissue and OA. [5][6][7] Leptin, being one of the extensively studied adipokines, is believed to play a role in the development of OA. [8][9][10] A noteworthy study conducted by Griffin et al revealed that, contrary to adipose tissue, leptin plays a substantial role in the development of knee OA in female C57BL/6J mice.…”

“…[ 4 ] Several studies have established a correlation between adipokines released by adipose tissue and OA. [ 5–7 ] Leptin, being one of the extensively studied adipokines, is believed to play a role in the development of OA. [ 8–10 ] A noteworthy study conducted by Griffin et al.…”

Analysis of the Level of Adiponectin and Selected Cytokines in Patients with Knee Osteoarthritis

“…Contrarily, in patients with rheumatoid arthritis, there were no observed significant correlations between adiponectin levels and plasma levels of cytokines [34]. Moreover, another study reported that elevated ACRP-30 levels promote IL-8 and IL-6 secretion in rheumatoid arthritis patients, suggesting that augmented adiponectin levels promote the illness [35].…”

Osteoarthritis, adipokines and the translational research potential in small animal patients

“…In addition to adipose tissue, adipokines are expressed in many other tissues. In recent years, the role of adipokines in the development and progression of OA has received increasing interest ( 12 , 13 ). At present, the known adipokines playing a role in the development and progression of OA include leptin, adiponectin, visfatin, resistin, progranulin, chemerin, lipocalin-2, vaspin, omentin-1 and nesfatin ( 14 , 15 ).…”

“…Adiponectin has been described as a primarily anti-inflammatory adipokine ( 14 ). Nevertheless, adiponectin also demonstrates pro-inflammatory characteristics and suppression of chondrocyte metabolism in OA ( 12 , 26 , 34 ). Total adiponectin was significantly increased in women with advanced knee OA ( 35 ).…”