ArticleCell reports2017
mTOR Inhibition Subdues Milk Disorder Caused by Maternal VLDLR Loss.
Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- VLDLR: A Multifunctional receptor in diverse pathophysiological processes.Cell communication and signaling : CCS · 2026Review
- Maternal Roughage Sources Influence the Gastrointestinal Development of Goat Kids by Modulating the Colonization of Gastrointestinal Microbiota.Animals : an open access journal from MDPI · 2025Article
- The histone methyltransferase ASH1L protects against bone loss by inhibiting osteoclastogenesis.Cell death and differentiation · 2024Article
- The Macrophage-Osteoclast Axis in Osteoimmunity and Osteo-Related Diseases.Frontiers in immunology · 2021Review
- STIM1 controls calcineurin/Akt/mTOR/NFATC2-mediated osteoclastogenesis induced by RANKL/M-CSF.Experimental and therapeutic medicine · 2020Article
- Molecular determinants for the polarization of macrophage and osteoclast.Seminars in immunopathology · 2019Review
- Milk lipid regulation at the maternal-offspring interface.Seminars in cell & developmental biology · 2018Review
- mTORC1 impedes osteoclast differentiation via calcineurin and NFATc1.Communications biology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
It is unknown whether and how very-low density lipoprotein receptors (VLDLRs) impact skeletal homeostasis. Here, we report that maternal and offspring VLDLRs play opposite roles in osteoclastogenesis and bone resorption. VLDLR deletion in the offspring augments osteoclast differentiation by enhancing RANKL signaling, leading to osteoporosis. In contrast, VLDLR deletion in the mother alters milk metabolism, which inhibits osteoclast differentiation and causes osteopetrosis in the offspring. The maternal effects are dominant. VLDLR-null lactating mammary gland exhibits higher mTORC1 signaling and cholesterol biosynthesis. Pharmacological probing reveals that rapamycin, but not statin, treatment of the VLDLR-null mother can prevent both the low bone resorption and our previously described inflammatory fur loss in their offspring. Genetic rescue reveals that maternal mTORC1 attenuation in adipocytes, but not in myeloid cells, prevents offspring osteopetrosis and fur loss. Our studies uncover functions of VLDLR and mTORC1 in lactation and osteoclastogenesis, illuminating key mechanisms and therapeutic insights for bone and metabolic diseases.
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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.