Rotator cuff tear repair poses significant challenges due to the complex gradient interface structure. In the face of disease-related disruptions in the tendon–bone interface (TBI), the strategy of constructing a biomimetic scaffold is a promising avenue. A novel 3D-printed rotator cuff scaffold loaded adipose stem cells (ADSCs), bone morphogenetic protein-2 (BMP-2), and collagen type I (COL I). The efficiency of the slow-release BMP-2 design depended on the dopamine-hyaluronic acid (HAD) and BMP-2 reaction. The cumulative release of BMP-2 was 44.97 ± 5.45% at 4 weeks. The 3D-printed bilayer scaffold, incorporating COL I and BMP-2, effectively promoted the differentiation of ADSCs into osteogenic, tenogenic, and chondrogenic lineages in vitro. The combination of 3D-printed bioactive scaffolds and ADSCs demonstrated a superior repair effect on rotator cuff injuries in vivo. Therefore, these findings indicates that the 3D-printed biomimetic scaffold loaded with ADSCs and BMP-2 holds potential as a promising graft for TBI healing.

Rotator cuff tears often require surgical reconstruction; however, outcomes remain suboptimal, primarily because of the challenges in fully restoring the tendon–bone interface (TBI). The normal fibrocartilaginous transition zone is often replaced by fibrous scar tissue, thereby increasing the risk of retears. A porous hyaluronic acid methacrylate hydrogel is developed to encapsulate adipose‐derived stem cells (ADSCs) and bone morphogenetic protein‐2 (BMP‐2). Gelatin microspheres served as porogens to create micropores within the hyaluronic acid methacrylate hydrogel (HMs), and hollow gelatin methacryloyl hydrogel microspheres are used to encapsulate BMP‐2 (GMBs). In vitro experiments confirm substantial proliferation and homing of ADSCs within the porous hydrogel system. When the ADSCs‐loaded composite hydrogel (HMs/MBs/ADSCs) is applied to a rat rotator cuff injury model, it effectively reconstructs the fibrocartilage transition zone and promotes TBI healing. Transcriptome sequencing is performed to elucidate the mechanisms underlying BMP‐2‐induced fibrocartilage reconstruction. Furthermore, integrated in vitro sequencing reveals that HMs/MBs/ADSCs modulated the tissue microenvironment to enhance tissue regeneration, primarily through BMP‐2′s regulation of the paracrine effects of ADSCs. This study explores the comprehensive pathway through which HMs/MBs/ADSCs enhance tissue regeneration, emphasizing the synergistic effects of BMP‐2 and ADSCs, and offers novel insights into the mechanisms underlying TBI healing.

Background: Acute skeletal muscle injuries are common among physical or sports traumas. The excessive oxidative stress at the site of injury impairs muscle regeneration. The authors have recently d... Plain language summary Muscle injuries are very common in daily life and in sports. When a muscle is injured, the local response inhibits the regeneration and differentiation of stem cells inside t...

Background: Volumetric Muscle Loss (VML) denotes the traumatic loss of skeletal muscle, a condition that can result in chronic functional impairment and even disability. While the body can naturally repair injured skeletal muscle within a limited scope, patients experiencing local and severe muscle loss due to VML surpass the compensatory capacity of the muscle itself. Currently, clinical treatments for VML are constrained and demonstrate minimal efficacy. Selenium, a recognized antioxidant, plays a crucial role in regulating cell differentiation, anti-inflammatory responses, and various other physiological functions. Methods: We engineered a porous Se@SiO₂ nanocomposite (SeNPs) with the purpose of releasing selenium continuously and gradually. This nanocomposite was subsequently combined with a decellularized extracellular matrix (dECM) to explore their collaborative protective and stimulatory effects on the myogenic differentiation of adipose-derived mesenchymal stem cells (ADSCs). The influence of dECM and NPs on the myogenic level, reactive oxygen species (ROS) production, and mitochondrial respiratory chain (MRC) activity of ADSCs was evaluated using Western Blot, ELISA, and Immunofluorescence assay. Results: Our findings demonstrate that the concurrent application of SeNPs and dECM effectively mitigates the apoptosis and intracellular ROS levels in ADSCs. Furthermore, the combination of dECM with SeNPs significantly upregulated the expression of key myogenic markers, including MYOD, MYOG, Desmin, and myosin heavy chain in ADSCs. Notably, this combination also led to an increase in both the number of mitochondria and the respiratory chain activity in ADSCs. Conclusion: The concurrent application of SeNPs and dECM effectively diminishes ROS production, boosts mitochondrial function, and stimulates the myogenic differentiation of ADSCs. This study lays the groundwork for future treatments of VML utilizing the combination of SeNPs and dECM.