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Article

An Additional Lrp4 High Bone Mass Mutation Mitigates the Sost-Knockout Phenotype in Mice by Increasing Bone Remodeling.

Calcified tissue international - 1 Feb 2024

Hendrickx Gretl, Boudin Eveline, Mateiu Ligia, Yorgan Timur A, Steenackers Ellen, Kneissel Michaela, Kramer Ina, Mortier Geert, Schinke Thorsten, Van Hul Wim

Abstract excerpt

Pathogenic variants disrupting the binding between sclerostin (encoded by SOST) and its receptor LRP4 have previously been described to cause sclerosteosis, a rare high bone mass disorder. The sclerostin-LRP4 complex inhibits canonical WNT signaling, a key pathway regulating osteoblastic bone formation and a promising therapeutic target for common bone disorders, such as osteoporosis. In the current study, we...

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Identifiers

PMID: 38051321
DOI: 10.1007/s00223-023-01158-0

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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An Additional Lrp4 High Bone Mass Mutation Mitigates the Sost-Knockout Phenotype in Mice by Increasing Bone Remodeling.PMID 38051321Read ↗

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