β-Diketone Functionalized Microspheres Chelate Reactive Iron via Metal Coordination for Cartilage Repair.

Excessive intracellular iron accumulation can induce mitochondrial dysfunction, leading to chondrocyte ferroptosis, a key contributor to cartilage damage in osteoarthritis (OA). Here, micelle-microfluidic hydrogel microspheres, featuring keto-enol-thiol bridged nano-sized secondary structures that disintegrate within the intracellular peroxidative environment to reveal β-diketone groups with metal chelation capabilities, are utilized for the in situ removal of reactive iron, thereby facilitating cartilage repair through the restoration of mitochondrial homeostasis. The relevant experiments demonstrate that the microspheres reduce iron influx by downregulating transferrin receptor (TfR1) expression and decrease mitochondrial iron uptake by upregulating mitochondrial outer membrane iron-sulfur cluster protein (CISD1), thus restoring intracellular mitochondrial iron homeostasis.

Three-dimensional gas-foamed scaffolds decorated with metal phenolic networks for cartilage regeneration.

Inflammation is a major impediment to the healing of cartilage injuries, yet bioactive scaffolds suitable for cartilage repair in inflammatory environments are extremely rare. Herein, we utilized electrospinning to fabricate a two-dimensional nanofiber scaffold (2DS), which was then subjected to gas foaming to obtain a three-dimensional scaffold (3DS). 3DS was modified with metal phenolic networks (MPNs) composed of epigallocatechin gallate (EGCG) and strontium ions (Sr) to afford a MPNs-modified 3D scaffold (3DS-E).

Mechanically tough, adhesive, self-healing hydrogel promotes annulus fibrosus repair via autologous cell recruitment and microenvironment regulation.

Annulus fibrosus (AF) defect is an important cause of disc re-herniation after discectomy. The self-regeneration ability of the AF is limited, and AF repair is always hindered by the inflammatory microenvironment after injury. Hydrogels represent one of the most promising materials for AF tissue engineering strategies.

Dietary intervention reprograms bone marrow cellular signaling in obese mice.

Objectives: The current study aimed to investigate the pathogenesis of obesity-induced impaired bone mass accrual and the impact of dietary intervention on bone density in the mouse model of obesity.

Methods: Mice were fed with chow diet (CD) for 10 months, high-fat-diet (HFD) for 10 months, or HFD for 6 months then transferred to chow diet for 4 months (HFDt).

Results: Weight loss and decreased intrahepatic lipid accumulation were observed in mice following dietary intervention.

Comparative proteomic analysis identifies differentially expressed proteins and reveals potential mechanisms of traumatic heterotopic ossification progression.

Background: Traumatic Heterotopic Ossification (tHO) is one of complications of elbow fractures to the detriment of patients' rehabilitation, and the severity of tHO corresponds to the size of ectopic bone. It has yet to be elucidated which proteins and pathways underlying the progression of tHO, and biomarkers to predict the severity of tHO at early stage of the disease also need further investigation.

Methods: In this study, a new rat model with distinct volume of ectopic bone was established first.

Exosomes for gene therapy effectively inhibit the endothelial-mesenchymal transition in mouse aortic endothelial cells.

Background: Heterotopic ossification (HO) can limit joint activity, causes ankylosis and impairs the function and rehabilitation of patients. Endothelial to mesenchymal transition (EndMT) plays an important role in the pathogenesis of HO, and high expression of SMAD7(Mothers Against Decapentaplegic Homolog 7) in endothelial cells can effectively reverse the TGF-β1 mediated EndMT. This article studied an appropriately engineered exosome with high biocompatibility and good targeting property to administrate SMAD7 gene therapy to inhibit the EndMT.