ArticleThe Journal of clinical investigation2019
Cathepsin K-deficient osteocytes prevent lactation-induced bone loss and parathyroid hormone suppression.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
53 citing papers in PubMed, 76 citations in OpenAlex.
- Increased Bone Resorption during Lactation in Pycnodysostosis.International journal of molecular sciences · 2021Trial
- Hypothalamic prolactin receptorNature communications · 2026Article
- Article
- MST4 as a key driver of osteoclast activation in osteoporosis.Journal of pharmaceutical analysis · 2026Article
- Inflammatory cytokines secreted from senescent periodontal ligament cells influence the osteocyte network in alveolar bone.JBMR plus · 2026Article
- Cathepsin K Alleviates Liver Fibrosis by Inhibiting the TGF-β/Smad Signaling Pathway and Inducing Hepatic Stellate Cell Apoptosis.Journal of clinical and translational hepatology · 2026Article
- Bone Metabolic Changes and Osteoporosis During Pregnancy and Lactation: A View from Dental Medicine.International journal of molecular sciences · 2025Review
- Estrogen loss activates memory T-cells to compromise bone integrity through distinct cortical compartments in mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Article
- Targeted Dual Microdroplets for Modulating Osteoclast Differentiation and Function: A Novel Therapeutic Approach to Combat Osteoporosis.ACS applied materials & interfaces · 2025Article
- Article
- Effect of High Glucose and Carboxymethyl-Lysine on Osteocyte Gene Expression.American journal of molecular biology · 2025Article
- Conditional Deletion of Gremlin-1 in Cathepsin K-expressing Mature Osteoclasts Altered the Skeletal Response to Calcium Depletion in Sex-Dependent Manner.Calcified tissue international · 2025Article
- Proteases and Osteoporosis: A Comprehensive Review of Their Role in Bone Health.Current drug targets · 2025Review
- Bidirectional crosstalk between the bone extracellular matrix and lysosomes in bone remodeling and osteoporosis.Frontiers in endocrinology · 2025Review
- Efferocytosis and Bone Dynamics.Current osteoporosis reports · 2024Review
- Article
- Connexin hemichannels drive lactation-induced osteocyte acidification and perilacunar-canalicular remodeling.Cell reports · 2024Article
- The osteocytic actions of glucocorticoids on bone mass, mechanical properties, or perilacunar remodeling outcomes are not rescued by PTH(1-34).Frontiers in endocrinology · 2024Article
- Current and future perspectives on pregnancy and lactation-associated osteoporosis.Frontiers in endocrinology · 2024Review
- Sfrp4 is required to maintain Ctsk-lineage periosteal stem cell niche function.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
Abstract
Lactation induces bone loss to provide sufficient calcium in the milk, a process that involves osteoclastic bone resorption but also osteocytes and perilacunar resorption. The exact mechanisms by which osteocytes contribute to bone loss remain elusive. Osteocytes express genes required in osteoclasts for bone resorption, including cathepsin K (Ctsk), and lactation elevates their expression. We show that Ctsk deletion in osteocytes prevented the increase in osteocyte lacunar area seen during lactation, as well as the effects of lactation to increase osteoclast numbers and decrease trabecular bone volume, cortical thickness and mechanical properties. In addition, Ctsk deletion in osteocytes increased bone Parathyroid Hormone related Peptide (PTHrP), prevented the decrease in serum Parathyroid Hormone (PTH) induced by lactation, but amplified the increase in serum 1,25(OH)2D. The net result of these changes is to maintain serum and milk calcium levels in the normal range, ensuring normal offspring skeletal development. Our studies confirm the fundamental role of osteocytic perilacunar remodeling in physiological states of lactation and provides genetic evidence that osteocyte-derived Ctsk contributes not only to osteocyte perilacunar remodeling, but also to the regulation of PTH, PTHrP, 1,25-Dyhydroxyvitamin D (1,25(OH)2D), osteoclastogenesis and bone loss in response to the high calcium demand associated with lactation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.