Fig. 8: Physiological tendon regeneration in neonatal mice requires the PI3K-Akt signalling pathway. | Nature Communications

Fig. 8: Physiological tendon regeneration in neonatal mice requires the PI3K-Akt signalling pathway.

From: PI3K-Akt signalling regulates Scx-lineage tenocytes and Tppp3-lineage paratenon sheath cells in neonatal tendon regeneration

Fig. 8: Physiological tendon regeneration in neonatal mice requires the PI3K-Akt signalling pathway.

When tendons are injured, regeneration is primarily mediated by tenocytes (Scx+ cells) and paratenon sheath cells (Tppp3+ cells). PI3K-Akt signalling pathway stimulates the proliferation and migration of these cell types. However, inactivation of the PI3K-Akt signalling pathway impairs cell proliferation and migration. In contrast, PI3K-Akt signalling regulates the stemness of both Scx+ and Tppp3+ cells. Inactivation of PI3K-Akt signalling leads to a loss of stemness and induces terminal differentiation into mature tenocytes. As a result, the neotendon fails to thicken, impairing functional and mechanical regeneration. Overall, the PI3K-Akt signalling pathway is necessary for physiological tendon regeneration in neonatal mice, and its inactivation alters the tendon regenerative potential.

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