Myotendinous Junction development and repair

progenitors, key MTJ developmental regulatory signals like Slit, Lrt, and BMP4, as well as MTJ decellularized ECM scaffolds or biomimetic 3D-printed scaffolds, will substantially enhance the efficacy of MTJ repair therapies. The Translational Potential of this Article: This review summarizes MTJ development across molecular linkages, signaling regulation, cellular composition, and tissue architecture, while assessing MTJ injury repair in terms of efficacy, mechanisms, limitations, and translational paths. Key barriers of MTJ repair include: conventional treatments (conservative and surgical) lacking high-quality data, RCTs, and unified guidelines for diverse patients; emerging approaches (bioactive factors, cell therapies, decellularized ECM scaffolds, tissue engineering) stuck at proof-of-concept or small-animal stages, without large-animal validation. It proposes establishing standardized cohorts, protocols, and parameters for conventional methods; accelerating large-animal safety/efficacy testing for emerging approaches to speed translation; constructing MTJ organoids based on key developmental cells and cues to provide a rapid drug testing platform for MTJ injury, thereby accelerating clinical translation; and integrating MTJ regulatory signals and stem/progenitor cells to enhance emerging therapy outcomes.