Table 2.
Types of cells, animal model, clinical data | Treatment for alteration cholesterol level | Regulated genes | Activity | Reference |
---|---|---|---|---|
Macrophages | Cholesterol | Increased IL6 | Increased osteoclast activity | (63) |
Osteoclast cells | Removal of cholesterol (by cyclodextrin or HDL) | Inhibited RANKL/CSF-1-induced osteoclast activity | (64) | |
Murine preosteoblast (CIMC4) | Removal of cholesterol (by cyclodextrin) | Inhibited RANKL | – | (66) |
Bone marrow-derived osteoclast | Removal of cholesterol (by cyclodextrin) | Inhibited V-ATPase | Inhibited osteoclast activity | (67) |
Human primary osteoblast cells | Atorvastatin | Increased OPG | Inhibited osteoclast activity | (70) |
Breast cancer and multiple myeloma | Simvastatin | Inhibited RANKL l-induced NFκB pathway | Inhibited RANKL-induced osteoclast | (75) |
Ovariectomized rat | Simvastatin | Decreased Trap | Decreased osteoclast | (73) |
Rat | High cholesterol | Increased Trap | Increased osteoclast | (74) |
Mice | High cholesterol | Increased osteoclast | (71) | |
Rabbit | High fat diet | Increased RANKL, MCP-1, Cathepsin K | Increased osteoclast | (72) |
Multiple myeloma patients | Simvastatin | Increased Trap (serum) | Bone resorption | (76) |
RANKL, receptor activator for nuclear factor kappa B ligand; OPG, osteoprotegerin; CSF-1, colony stimulating factor-1; Trap, tartrate resistant acid phosphatase; MCP-1, monocyte chemoattractant protein-1.