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RIPK4 in Osteolineage cells regulate bone and bone marrow homeostasis via MFN2

GSE243610 Mus musculus Expression profiling by high throughput sequencing 8 samples Submitted 2025/05/19 Platform GPL24247
Summary
Human RIPK4 mutation leads to Bartsocas-Papas syndrome (BPS), characterized by severe craniofacial, skin and limb abnormalities. However, how RIPK4 regulates skeletal system development remains largely elusive. Herein, using global RIPK4 ablation mice model, we demonstrated that RIPK4 deficiency caused musculoskeletal disorders including severe osteoporosis, kyphosis, sarcopenia and induced myeloid-biased hematopoiesis and subsequently altered peripheral immune responses. Further detailed investigation confirmed that osteolineage RIPK4, not epidermal RIPK4, regulated the osteogenesis and bone marrow myelopoiesis via MFN2. These findings deciphered the essential role of RIPK4 in maintaining skeletal homeostasis and unveiled an unappreciated mechanism of RIPK4-MFN2 axis in regulating osteogenesis and bone marrow myelopoiesis.
Published in
RIPK4-mediated MFN2 degradation drives osteogenesis through mitochondrial fragmentation and restricts myelopoiesis by blocking mitochondrial transfer
Ding P, Wang X, Gao C et al. · Nature communications 2025 · PMID 40683865 · doi:10.1038/s41467-025-61808-9
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Also filed as BioProject PRJNA1019230 and SRA study SRP461914. Searching any of these in the dataset finder brings you back here.

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