ArticleGenes & diseases2025
Progranulin deficiency associates with postmenopausal osteoporosis via increasing ubiquitination of estrogen receptor α.
Article in Genes & diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Unveiling estrogen's role: a comprehensive review of its impact on skin health and disease.Apoptosis : an international journal on programmed cell death · 2026Review
- Linear Association of Derivatives of Triglyceride-Glucose Index with Incident Lower Limb Joint Pain in Middle-Aged and Older Chinese Adults: A Prospective Cohort Study.Journal of pain research · 2026Article
- Context-dependent roles of 11β-HSD1 in bone and skeletal muscle diseases.American journal of translational research · 2026Review
- Unraveling the mechanisms of nicotine-induced osteoporosis via network toxicology, bioinformatics, and molecular docking.Tobacco induced diseases · 2026Article
- Molecular mechanisms and targeted therapy of progranulin in metabolic diseases.Frontiers in endocrinology · 2025Review
- IMPC-based screening revealed thatFrontiers in cell and developmental biology · 2024Article
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Authors and funding
15 authors.
Funding
Abstract
Estrogen deficiency is considered the most important cause of postmenopausal osteoporosis. However, the underlying mechanism is still not completely understood. In this study, progranulin (PGRN) was isolated as a key regulator of bone mineral density in postmenopausal women through high throughput proteomics screening. In addition, PGRN-deficient mice exhibited significantly lower bone mass than their littermates in an ovariectomy-induced osteoporosis model. Furthermore, estrogen-mediated inhibition of osteoclastogenesis and bone resorption as well as its protection against ovariectomy-induced bone loss largely depended on PGRN. Mechanistic studies revealed the existence of a positive feedback regulatory loop between PGRN and estrogen signaling. In addition, loss of PGRN led to the reduction of estrogen receptor α, the important estrogen receptor involved in estrogen regulation of osteoporosis, through enhancing its degradation via K48-linked ubiquitination. These findings not only provide a previously unrecognized interplay between PGRN and estrogen signaling in regulating osteoclastogenesis and osteoporosis but may also present a new therapeutic approach for the prevention and treatment of postmenopausal osteoporosis by targeting PGRN/estrogen receptor α.
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