ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Piezo2
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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12 authors.
Funding
Abstract
Heterotopic ossification (HO) of the Achilles tendon induces pain and impairs tendon mechanical function, yet its pathogenic mechanisms remain largely unknown. Given that neurotransmitters, inflammatory cytokines, and mechanical loading are highly associated with HO incidence, we raised a hypothesis that activation of sensory neurons within the injured Achilles tendon may be one critical cause driving HO progression. This present work demonstrates that Netrin-1, predominantly secreted by macrophages at the injured site, profoundly promotes the regeneration of Piezo2-expressing sensory nerves in the Achilles tendon of mice after puncture. This is accompanied by an aberrant rise in the pro-osteogenic neuropeptide calcitonin gene-related peptide (CGRP) in both sensory nerves at the injury site and the dorsal root ganglion (DRG), particularly under the synergistic influence of mechanical stimulation and prostaglandin E2 (PGE2), a pro-inflammatory cytokine initially produced by macrophages. Consequently, osteogenic differentiation of tendon-derived stem cells (TDSCs) is enhanced, which in turn further stimulates PGE2 secretion from osteoblasts. Of note, such an effect and subsequent HO formation can be significantly attenuated by tail suspension treatment or by blocking signaling pathways mediated by CGRP, Netrin-1, PGE2, or Piezo2. Together, these findings elucidate the crosstalk among macrophages, osteoblasts, and Piezo2
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