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During the bone fracture healing process, the new tissue is characterized by high fragility and delicacy, which exposes it to slower regeneration or additional damage

The interaction between vascular ECs and vascular smooth muscle cells occurs directly, through main crosstalk mechanisms: paracrine regulation by bioactive molecules, communication via gap junctions, or information transfer via extracellular vesicles or extracellular matrix (ECM) [36]

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Unlike systemic growth hormone stimulation, this activity appears localized to mechanically stressed tissue