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The myotendinous junction (MTJ) acts as a bridge between muscle and tendon; yet its high stiffness relative to muscle fibers renders the tissue susceptible to injuries due to eccentric loading disparities. The limited regenerative capacity of MTJ tissue and potential for postsurgical scarring and reinjury necessitates complementary therapeutics that can enhance cellular interactions, restore mechanical properties, and support tissue rehabilitation. This review explores various approaches to engineer the MTJ utilizing biomaterial scaffolds and cellularized materials that mimic structure and function. While biomimetic materials show promise, challenges remain due to the interface’s complexity and differing patient- and location-specific structure–function characteristics, necessitating further research to address these gaps. This review also highlights the importance of studying MTJ injuries in women’s health and craniofacial reconstruction. Furthermore, engineered MTJ models provide versatile platforms for investigating trauma and degeneration, thus offering potential for advancing research across multiple fields, shedding light on interactions at tissue interfaces, and shaping the future of MTJ rehabilitation. 

This article shows how mitochondria in murine cardiac changes, importantly elucidating age-related changes. It also is the first to show that the MICOS complex may play a role in outer membrane mitochondrial structure. 

Abstract During aging, muscle gradually undergoes sarcopenia, the loss of function associated with loss of mass, strength, endurance, and oxidative capacity. However, the 3D structural alterations of mitochondria associated with aging in skeletal muscle and cardiac tissues are not well described. Although mitochondrial aging is associated with decreased mitochondrial capacity, the genes responsible for the morphological changes in mitochondria during aging are poorly characterized. We measured changes in mitochondrial morphology in aged murine gastrocnemius, soleus, and cardiac tissues using serial block‐face scanning electron microscopy and 3D reconstructions. We also used reverse transcriptase‐quantitative PCR, transmission electron microscopy quantification, Seahorse analysis, and metabolomics and lipidomics to measure changes in mitochondrial morphology and function after loss of mitochondria contact site and cristae organizing system (MICOS) complex genes,Chchd3,Chchd6, andMitofilin. We identified significant changes in mitochondrial size in aged murine gastrocnemius, soleus, and cardiac tissues. We found that both age‐related loss of the MICOS complex and knockouts of MICOS genes in mice altered mitochondrial morphology. Given the critical role of mitochondria in maintaining cellular metabolism, we characterized the metabolomes and lipidomes of young and aged mouse tissues, which showed profound alterations consistent with changes in membrane integrity, supporting our observations of age‐related changes in muscle tissues. We found a relationship between changes in the MICOS complex and aging. Thus, it is important to understand the mechanisms that underlie the tissue‐dependent 3D mitochondrial phenotypic changes that occur in aging and the evolutionary conservation of these mechanisms betweenDrosophilaand mammals.