Osteoporosis is the most prevalent systemic skeletal system disease, leading to increased bone fragility and vulnerability to fractures. Due to the microarchitectural destruction in bone tissue, fracture healing in osteoporoti patients is often delayed and compromised compared with non‑osteoporotic individuals. Osteoporosis usually results from meno‑ pause, aging, metabolic diseases and drug therapies with the precise cellular and molecular mechanism remaining to be elucidated.
Recent studies have shown that four peptides (BPC-157, AOD 9604, MOTS-c, Peptide 11R‐VIVIT) have been proven to have healing effects for such disease in several types of model… High concentration and long-term stimulation of TGF-β1 induced osteogenic differentiation of bone marrow mesenchymal stem cells (MSCs) in vitr2. TGF-β pathway-related genes exert anti-osteoporosis effects by regulating the function of bone deposits and osteoclasts. TGF-β also affects the bone formation by promoting the proliferation and differentiation of osteoblasts, as well as the synthesis of extracellular matrix.
