The levels of inflammatory factors, TNF-α, interleukin-6 (IL-6) and C-reactive protein (CRP), in patients without complicating osteoporosis were significantly lower than those in patients complicated with osteoporosis.
Additional analysis revealed that let-7a, a microRNA induced by TNF-α in osteoporosis, inhibited the expression of the Fas/FasL system via post-transcriptional regulation.
Together, these results demonstrate that TNF-α synergistically promotes RANKL-induced osteoclasts formation through activation of PI3K/Akt signaling, which ultimately contributes to osteoporosis syndrome in postmenopausal women.
TNF and its signal pathway remains an important target for the development of new therapies for bone loss from osteoporosis and inflammatory arthritis.
Duration of diabetes mellitus (DM) and levels of glycosylated hemoglobin A1c (HbA1c), fasting plasma glucose (FPG) and fasting insulin (FINS) level, levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6), level of 24h urine protein (24hndb) of patients in the combination with osteoporosis group was significantly higher, while the value of eGFR was lower than that of patients in the non-combination with osteoporosis group.
Compound mouse mutants generated by genetically deleting the Tnfα gene on a Tshr(-/-) (homozygote) or Tshr(+/-) (heterozygote) background resulted in full rescue of the osteoporosis, low bone formation, and hyperresorption that accompany TSH deficiency.
<b>Objectives:</b> We explored the interactions of osteoprotegerin (OPG) with biomarkers of bone turnover and cytokines, including soluble receptor activator for nuclear factor kappa beta ligand (sRANKL), tumor necrosis factor-related apoptosis-induced ligand (TRAIL), and Wnt inhibitors in osteoporosis, vasculopathy and fibrosis related to systemic sclerosis (SSc).
Tumor necrosis factor (TNF) superfamily member 11 (TNFSF11, also known as RANKL) regulates multiple physiological or pathological functions, including osteoclast differentiation and osteoporosis.
In conclusion, NK3 and NK49 may simultaneously alleviate BV and osteoporosis by suppressing NF-<i>κ</i>B-linked TNF-<i>α</i> expression through the regulation of gut microbiota population.
The inhibited osteogenic differentiation of BMSCs undergoing TNF-α induction is improved by resveratrol treatment, which contributes to alleviate the progression of osteoporosis.
These TNF family members not only regulate physiological bone remodeling but they are also implicated in the pathogenesis of various bone diseases such as osteoporosis and bone loss in inflammatory conditions.
The concentrations of CTX (266.61 ± 64.65 vs 293.09 ± 72.34 vs 235.48 ± 62.85, P < 0.05), IL-6 (44.36 ± 6.45 vs 48.05 ± 8.04 vs 39.06 ± 7.95, P < 0.05) and TNF-α (30.53 ± 6.28 vs 34.52 ± 7.15 vs 28.66 ± 6.19, P < 0.01) in the hypertension group and in the H-type hypertension group were significantly higher than those in the osteoporosis group.
OPG belongs to the tumor necrosis factor receptor superfamily, which plays a crucial role in bone remodeling and is thus a promising candidate gene of osteoporosis.
The results showed that the levels of miR‑144, Sfrp1 and TNF‑α in clinical serum samples obtained from patients with postmenopausal OP were higher than those in serum samples obtained from postmenopausal women with normal bone density.
We aimed to determine whether tumor necrosis factor inhibitors (TNFi) have beneficial effects on bone mineral density (BMD) in rheumatoid arthritis (RA) patients with osteoporosis receiving bisphosphonate.
In addition, short hairpin RNA TRPV4-lentivirus administration significantly diminished the increased levels of several osteoclastogenesis-related genes (RANKL, TRAP, and tumor necrosis factor-α), alleviated the disturbed microarchitecture of lumbar vertebrae, restored the decreased bone mineral density, ratio of bone volume to total tissue volume, trabecular thickness, and trabecular number, and diminished the increased trabecular separation, in ovariectomy (OVX)-induced osteoporosis mice.