ArticleCell & bioscience2022
BHLHE40 promotes osteoclastogenesis and abnormal bone resorption via c-Fos/NFATc1.
Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- Modulation of bone homeostasis by dual drug-loaded premixed magnesium tri-magnesium phosphate bone cement for the treatment of osteoporotic vertebral compression fractures.Bioactive materials · 2025Article
- BPAG1 promotes osteoclastogenesis and postmenopausal osteoporosis via activating ERK signaling pathway.iScience · 2025Article
- Integrative genomic analysis and diagnostic modeling of osteoporosis: unraveling the interplay of autophagy, osteogenesis, adipogenesis, and immune infiltration.Frontiers in medicine · 2025Article
- IGF-II regulates lysyl oxidase propeptide and mediates its effects in part via basic helix-loop-helix E40.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- The bone nonunion microenvironment: A place where osteogenesis struggles with osteoclastic capacity.Heliyon · 2024Review
- Basic-helix-loop-helix family member e41 suppresses osteoclastogenesis and abnormal bone resorption disease via NFATc1.iScience · 2024Article
- A Recombinant Parathyroid Hormone-Related Peptide Locally Applied in Osteoporotic Bone Defect.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Strontium Ranelate Inhibits Osteoclastogenesis through NF-κB-Pathway-Dependent Autophagy.Bioengineering (Basel, Switzerland) · 2023Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDysregulated osteoclast activity due to altered osteoclast differentiation causes multiple bone diseases. Osteoclasts are multinucleated giant cells derived from hematopoietic stem cells and play a major role in bone absorption. However, the mechanisms underlying the tight regulation of osteoclast differentiation in multiple pathophysiological status remain unknown.
resultsWe showed that Bhlhe40 upregulation is tightly associated with osteoclast differentiation and osteoporosis. Functionally, Bhlhe40 promoted osteoclast differentiation in vitro, and Bhlhe40 deficiency led to increased bone mass and decreased osteoclast differentiation in vivo. Moreover, Bhlhe40 deficient mice resisted estrogen deficiency and aging-induced osteoporosis. Mechanism study showed that the increase in bone mass due to Bhlhe40 deficiency was a cell intrinsic defect in osteoclast differentiation in these mice. BHLHE40 upregulated the gene expression of Fos and Nfatc1 by directly binding to their promoter regions. Notably, inhibition of Fos/Nfatc1 abrogated the enhanced osteoclast differentiation induced by BHLHE40 overexpression.
conclusionsOur research reveals a novel Bhlhe40/c-Fos/Nfatc1 axis involved in regulating osteoclastogenesis and shows that osteoporosis caused by estrogen deficiency and aging can be rescued by regulating Bhlhe40 in mice. This may help in the development of a new strategy for the treatment of osteoporosis.
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