Piezo1, Integrins, and YAP/TAZ in Osteoporotic Mechanotransduction: Key Pathways, Crosstalk, and Therapeutic Implications.
Level 5 - mechanism / opinion, no new human data
Narrative review of molecular mechanisms with no primary human data.
PubMed 42503528 · doi:10.1007/s00223-026-01584-w
What was done
This review synthesized literature on the molecular mechanisms governing bone mechanotransduction, focusing on the roles, hierarchy, and crosstalk among the mechanosensitive ion channel Piezo1, cell-matrix adhesion receptors (integrins), and transcriptional co-activators (YAP/TAZ) across osteocytes, osteoblasts, bone marrow mesenchymal stem cells, and osteoclasts.
What was found
The abstract provides no quantitative data or numerical findings. It outlines that Piezo1 (mediating calcium-dependent signaling), integrins (mediating focal adhesion force transduction), and YAP/TAZ (mediating nuclear transcriptional programs) operate in a dynamic membrane-to-nucleus signaling axis implicated in age-related, postmenopausal, and unloading-induced bone loss.
Why it matters
Mapping the crosstalk among Piezo1, integrins, and YAP/TAZ helps clarify how physical unloading drives skeletal fragility and identifies molecular targets for pharmacological, biomaterial, and mechanically assisted osteoporosis interventions.
Limits
The abstract reports no original experimental data, quantitative synthesis, or systematic search criteria. Described pathways rely primarily on preclinical models, and context-dependent controversies remain regarding their direct clinical translation in humans.
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- context Ceasing estrogen replacement therapy results in a rapid decline in bone mineral density because estrogen is the primary transducing signal that couples mechanical bone loading to osteoblast and osteoclast activity.