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GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation
Weiqing Liu1, Liyan Zhou1, Chenchen Zhou1
1State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China.
Abstract:
Osteoporosis is an age-related disease that affects millions of people. Growth differentiation factor 11 (GDF11) is a secreted member of the transforming growth factor beta (TGF-β) superfamily. Deletion of Gdf11 has been shown to result in a skeletal anterior-posterior patterning disorder. Here we show a role for GDF11 in bone remodelling. GDF11 treatment leads to bone loss in both young and aged mice. GDF11 inhibits osteoblast differentiation and also stimulates RANKL-induced osteoclastogenesis through Smad2/3 and c-Fos-dependent induction of Nfatc1. Injection of GDF11 impairs bone regeneration in mice and blocking GDF11 function prevents oestrogen-deficiency-induced bone loss and ameliorates age-related osteoporosis. Our data demonstrate that GDF11 is a previously unrecognized regulator of bone remodelling and suggest that GDF11 is a potential target for treatment of osteoporosis.
Insights
Growth differentiation factor 11 (GDF11) accelerates bone loss by inhibiting bone formation and promoting bone resorption. Blocking GDF11 may be a new strategy for treating osteoporosis.
Area of Science:
- Bone Biology
- Endocrinology
- Skeletal Biology
Background:
- Osteoporosis is a prevalent age-related condition impacting bone health.
- Growth differentiation factor 11 (GDF11), a TGF-β superfamily member, is implicated in skeletal development.
- Previous research indicated Gdf11 deletion causes skeletal patterning defects.
Purpose of the Study:
- To investigate the role of GDF11 in adult bone remodeling.
- To determine the effects of GDF11 on bone formation and resorption.
- To explore GDF11 as a potential therapeutic target for osteoporosis.
Main Methods:
- Administration of GDF11 to young and aged mice.
- Assessment of osteoblast differentiation and osteoclastogenesis.
- Evaluation of GDF11's impact on bone regeneration and osteoporosis models.
Main Results:
- GDF11 treatment induced bone loss in mice.
- GDF11 inhibited osteoblast differentiation and stimulated osteoclastogenesis.
- Blocking GDF11 prevented bone loss in osteoporosis models.
Conclusions:
- GDF11 is a novel regulator of bone remodeling.
- GDF11 promotes bone loss through effects on osteoblasts and osteoclasts.
- Targeting GDF11 presents a potential therapeutic avenue for osteoporosis.
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