HIF1α is required for osteoclast activation by estrogen deficiency in postmenopausal osteoporosis.

Proc Natl Acad Sci U S A

Departments of Orthopedic Surgery, Integrated Bone Metabolism and Immunology, and Musculoskeletal Reconstruction and Regeneration Surgery, Keio Kanrinmaru Project, and Department of Dentistry and Oral Surgery, School of Medicine, Keio University, Tokyo 160-8582, Japan.

Published: October 2013

In women, estrogen deficiency after menopause frequently accelerates osteoclastic bone resorption, leading to osteoporosis, the most common skeletal disorder. However, mechanisms underlying osteoporosis resulting from estrogen deficiency remain largely unknown. Here we show that in bone-resorbing osteoclasts, estrogen-dependent destabilization of hypoxia-inducible factor 1 alpha (HIF1α), which is unstable in the presence of oxygen, plays a pivotal role in promoting bone loss in estrogen-deficient conditions. In vitro, HIF1α was destabilized by estrogen treatment even in hypoxic conditions, and estrogen loss in ovariectomized (Ovx) mice stabilized HIF1α in osteoclasts and promoted their activation and subsequent bone loss in vivo. Osteoclast-specific HIF1α inactivation antagonized bone loss in Ovx mice and osteoclast-specific estrogen receptor alpha deficient mice, both models of estrogen-deficient osteoporosis. Oral administration of a HIF1α inhibitor protected Ovx mice from osteoclast activation and bone loss. Thus, HIF1α represents a promising therapeutic target in osteoporosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799362PMC
http://dx.doi.org/10.1073/pnas.1308755110DOI Listing

Publication Analysis

Top Keywords

bone loss
16
estrogen deficiency
12
ovx mice
12
osteoclast activation
8
hif1α
7
estrogen
6
osteoporosis
5
bone
5
loss
5
hif1α required
4

Similar Publications

To investigate the population distribution characteristics of elderly osteoporosis fracture patients in Hebei Province and analyze the effects of air pollutants on elderly osteoporosis fractures, We retrospectively collected 18,933 cases of elderly osteoporosis fractures from January 1, 2019, to December 31, 2022, from four hospitals in Hebei Province. The average age was 76.44 ± 7.

View Article and Find Full Text PDF

The potential for mitigating intestinal inflammation through the gut-bone axis in the treatment of osteoporosis is significant. While various gut-derived postbiotics or bacterial metabolites have been created as dietary supplements to prevent or reverse bone loss, their efficacy and safety still need improvement. Herein, a colon-targeted drug delivery system is developed using surface engineering of polyvinyl butyrate nanoparticles by shellac resin to achieve sustained release of postbiotics butyric acid at the colorectal site.

View Article and Find Full Text PDF

METTL14 Mediates m6A methylation to improve osteogenesis under oxidative stress condition.

Redox Rep

December 2025

Department of Clinical Laboratory, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai, People's Republic of China.

Objectives: Bone remodeling imbalance contributes to osteoporosis. Though current medications enhance osteoblast involvement in bone formation, the underlying pathways remain unclear. This study was aimed to explore the pathways involved in bone formation by osteoblasts, we investigate the protective role of glycolysis and N6-methyladenosine methylation (m6A) against oxidative stress-induced impairment of osteogenesis in MC3T3-E1 cells.

View Article and Find Full Text PDF

Background: Emerging research indicates that gut microbiota (GM) are pivotal in the regulation of immune-mediated bone diseases. Nonunion, a bone metabolic disorder, has an unclear causal relationship with GM and immune cells. This study aims to elucidate the causal relationship between GM and nonunion using Mendelian Randomization (MR) and to explore the mediating role of immune cells.

View Article and Find Full Text PDF

Heterodisomy in the locus is also a cause of pseudohypoparathyroidism type 1B (iPPSD3).

Front Endocrinol (Lausanne)

December 2024

Rare Disease Research Group, Molecular (Epi) Genetics Laboratory, Bioaraba Health Research Institute, Araba University Hospital, Vitoria-Gasteiz, Spain.

Objective: To identify the genetic cause underlying the methylation defect in a patient with clinical suspicion of PHP1B/iPPSD3.

Design: Imprinting is an epigenetic mechanism that allows the regulation of gene expression. The locus is one of the loci within the genome that is imprinted.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!