Lipid Metabolism in Cartilage Development, Degeneration, and Regeneration

Abstract

Lipids affect cartilage growth, injury, and regeneration in diverse ways. Diet and metabolism have become increasingly important as the prevalence of obesity has risen. Proper lipid supplementation in the diet contributes to the preservation of cartilage function, whereas excessive lipid buildup is detrimental to cartilage. Lipid metabolic pathways can generate proinflammatory substances that are crucial to the development and management of osteoarthritis (OA). Lipid metabolism is a complicated metabolic process involving several regulatory systems, and lipid metabolites influence different features of cartilage. In this review, we examine the current knowledge about cartilage growth, degeneration, and regeneration processes, as well as the most recent research on the significance of lipids and their metabolism in cartilage, including the extracellular matrix and chondrocytes. An in-depth examination of the involvement of lipid metabolism in cartilage metabolism will provide insight into cartilage metabolism and lead to the development of new treatment techniques for metabolic cartilage damage.

Serum lipid biomarkers and inflammatory cytokines associated with onset and clinical status of patients with early knee osteoarthritis

“…In addition, when there is an aggregation of joint cholesterol, vascular injury is at risk, resulting in impaired blood flow to the subchondral bone. When cartilage loses oxygen and nutrients, this can result in histopathology and contribute to the development of OA ( 48 , 49 ). Additionally, hypercholesterolemia can also lead to oxidation and lipid deposition in tissues, resulting in cartilage damage ( 49 ).…”

“…When cartilage loses oxygen and nutrients, this can result in histopathology and contribute to the development of OA ( 48 , 49 ). Additionally, hypercholesterolemia can also lead to oxidation and lipid deposition in tissues, resulting in cartilage damage ( 49 ). Our results showed higher levels of total cholesterol in patients with EOA and a correlation between these levels and a greater intensity of pain and disability, showing a possible relationship between cholesterol and the genesis of OA (metabolic OA phenotype).…”

Decreased expression of ATP‐binding cassette protein G1 promotes abnormal adipogenesis of condylar chondrocytes in temporomandibular joint osteoarthritis

“…5 In recent years, studies have shown that abnormal lipid metabolism is involved in the development of knee OA. 6,7 Notable changes in adipogenesis of knee OA chondrocytes are observed, and the ability of adipogenic chondrocytes to secrete matrix degradation factors is enhanced. [8][9][10] We previously found that in the degenerated condylar cartilage of mice with TMJ OA induced by abnormal occlusion, chondrocytes showed notable changes in adipogenesis.…”

“…As the only cell type in TMJ condylar cartilage, condylar chondrocytes play a critical role in cartilage degeneration, but their specific mechanism remains to be clarified 5 . In recent years, studies have shown that abnormal lipid metabolism is involved in the development of knee OA 6,7 . Notable changes in adipogenesis of knee OA chondrocytes are observed, and the ability of adipogenic chondrocytes to secrete matrix degradation factors is enhanced 8–10 .…”

Oleanolic acid, a small-molecule natural product, inhibits ECM degeneration in osteoarthritis by regulating the Hippo/YAP and Wnt/β-catenin pathways

“…8 It is becoming increasingly evident that degenerative mechanisms of cartilage extracellular matrix (ECM) play a central role in regulating the effects of biomechanical disorders of joint tissues. 9 In osteoarthritic cartilage, inflammatory factors induce the expression of matrix metalloproteinases (MMPs) and a disintegrin and MMP with thrombospondin motifs (ADAMTS), and their increase leads to the breakdown of cartilage ECM components and damage to articular cartilage, thus aggravating the development of OA. 10 Therefore, strategies to inhibit catabolic factors leading to cartilage degradation may be promising in the treatment of OA.…”