Table 3.
Cellular studies on the association between lipid metabolism and OA.
| First authors (year) | Cell type | Stimulant | Signaling pathway | Effect on OA |
|---|---|---|---|---|
| Liao (2023) [98] | Primary rat fibroblast-like synoviocytes | Lipopolysaccharide; L-carnitine | AMPK-ACC-CPTI | Pro-inflammatory; synovial protective effects |
| Ma (2022) [112] | Human OA chondrocytes | Palmitic acid | NF-κB | Activated NF-κB; upregulated inducible nitric oxide synthase, cyclooxygenase-2, prostaglandin E2, and nitric oxide; degraded extracellular matrix |
| Villalvilla (2020) [81] | OA articular chondrocytes | Oxidized low-density lipoprotein | / | Modified pro-inflammatory and catabolic gene and protein expression |
| Chen (2020) [83] | OA-SFs | Resistin | PKC, p38, and JNK | Resistin inhibited miR-381 |
| Tsai (2020) [77] | OA-SFs | Visfatin short hairpin RNA | PI3K/Akt | Visfatin inhibited miR-485-5p |
| Sun (2023) [134] | Human chondrocytes | Palmitic acid; xanthohumol | AMPK and NF-κB | Obesity-related OA; decreased cartilage matrix degradation induced by palmitic acid |
| Li (2023) [72] | Human and mouse chondrocytes | Cholesterol; circARPC1B | / | Downregulated circARPC1B; preserved the extracellular matrix |
| Gong (2023) [141] | Human and mouse chondrocytes | Doxorubicin | PI3K/Akt | Induce chondrocyte senescence |
| Yang (2023) [138] | Human C28/I2 chondrocytes | Andrographolide | NF-κB | Reduced reactive oxygen species generation and activated ADAMTS4 |
| Primrose (2023) [118] | Human chondrocytes | Leptin | / | Reduced levels of HES1; increased levels of ADAMTS5 and MMP13 |
| Yamamoto (2022) [84] | LRP1-deficient fibroblasts and human chondrocytes | Soluble LRP1-II | / | Increased the levels of slit guidance ligand 2, ADAMTS1, and TNF-inducible gene 6 in the chondrocyte medium |
| Sanchez (2022) [135] | Primary OA chondrocytes | Curcuma longa; Boswellia serrata | Nrf2; Nrf1; PPARα | Anti-oxidative, anti-inflammatory, and anti-catabolic effects |
| Wang (2022) [114] | Primary rat condylar chondrocytes | Fluid flow shear stress | PPARγ | Inhibited adipogenesis of chondrocytes and cartilage degeneration |
| Jin (2022) [133] | SW1353 chondrosarcoma cells | Lipopolysaccharides; fatty acids | TLR4/NF-κB | Mimicked OA status in vitro; affected chondrocyte pyroptosis |
| Liu (2022) [130] | Primary mouse chondrocytes | Acetyl-CoA carboxylase inhibitor | / | Ameliorated lipid accumulation in chondrocytes |
| Zhao (2022) [126] | Human chondrocytes | Resistin | p38-MAPK; NF-κB | Upregulated pro-inflammatory cytokines and matrix-degrading enzymes |
| Wei (2022) [119] | Primary OA rat chondrocytes | Leptin | / | Significantly increased lysyl oxidase-like 3, inhibited autophagy |
| Mao (2021) [137] | ATDC5 cells | IL-1β; PPARγ inhibitor | / | Inflammation, apoptosis, and extracellular matrix degradation |
| Wang (2022) [113] | C28I2 cells | Digoxin | / | Increased the expressions of two markers of anabolism |
| Papageorgiou (2021) [136] | OA chondrocytes | Resveratrol | NF-κB | Induction of autophagy |
| Chang (2021) [125] | Human OA chondrocytes | Visfatin | p38 | Decreased intracellular elasticity and viscosity |
| Philp (2021) [124] | Human OA chondrocytes | Visfatin | / | Cartilage matrix degradation |
| Cheleschi (2021) [127] | Human OA chondrocytes | Hydrostatic pressure; visfatin | / | Cartilage matrix degradation |
| Harasymowicz (2021) [120] | Human OA chondrocytes | Adiponectin | / | Cartilage degeneration |
| Law (2020) [123] | OA-SFs | Visfatin | p38; AMPK | Enhanced adhesion of monocytes to OA-SFs |
| Chang (2020) [115] | OA-SFs | Apelin | PI3K; ERK | Pro-inflammatory |
| Gu (2020) [131] | Human SW1353 chondrocytes | AGEs; GW9508 | NF-κB | Decreased free fatty acid receptor 1; suppressed inflammation and NF-κB activation |
| Chai (2020) [129] | Human SW1353 chondrocytes | IL-1β; omentin-1 | / | G1 phase cell-cycle arrest; protection of chondrocytes from senescence |
| Frommer (2019) [118] | Primary human and murine osteoblasts | Free fatty acids | TLR4 | Subchondral bone damage in OA |
| Cheleschi (2019) [122] | Human OA synoviocytes | Visfatin; resistin | NF-κB | Induced apoptosis and superoxide production |
| Zhuo (2019) [128] | Human SW1353 chondrocytes | TNF-α; INT-777 | p38; NF-κB | Abnormal loss of extracellular matrix; reduced extracellular matrix degradation |
| Cheleschi (2019) [121] | Human OA chondrocytes | Visfatin | NF-κB | Induce apoptosis and oxidative stress |
| Zhang (2019) [116] | ATDC5 cells | Leptin | / | Stimulate hypertrophic differentiation of ATDC5 cells |
| Belenska-Todorova (2021) [102] | Bone marrow-derived cells | Metformin and alendronate | / | Inhibited the expression of RANK and RANKL on osteoblasts and osteoclasts and fibroblast differentiation |
| Nogueira-Recalde (2019) [139] | T/C28a2 chondrocytes | IL-6; fenofibrate | PPARα | Induced senescence; reduced the number of senescent cells |
| Vaamonde-Garcia (2019) [140] | Human OA-SFs | TGF-β1; prednisolone and/or 15d-PGJ2 | PPAR-γ | Pro-fibrotic; anti-fibrotic |
ACC: acetyl-CoA carboxylase; ADAMTS: a disintegrin and metalloproteinase with thrombospondin motifs; AGEs: advanced glycation end products; AMPK: AMP-activated protein kinase; CPTI: carnitine palmitoyltransferase I; ERK: extracellular signal-regulated kinase; 15d-PGJ2: 15-deoxy-Δ-12,14-prostaglandin J2; IL: interleukin; JNK: c-Jun N-terminal kinase LRP: low-density lipoprotein receptor-related protein; MAPK: mitogen-activated protein kinase; MMP: matrix metalloproteinase; NF: nuclear factor; OA: osteoarthritis; OA-SF: osteoarthritis synovial fibroblast; PI3K: phosphoinositide 3-kinase; PKC: protein kinase C; PPAR: peroxisome proliferator-activated receptor; RANK: receptor activator of NF-κB; RANKL: receptor activator of NF-κB ligand; TGF-β1: transforming growth factor-beta 1; TLR: Toll-like receptor; TNF: tumour necrosis factor.