Exosomes (Exos) are extracellular vesicles secreted by cells and serve as crucial mediators of intercellular communication. They play a pivotal role in the pathogenesis and progression of various diseases and offer promising avenues for therapeutic interventions. Exos derived from mesenchymal stem cells (MSCs) have significant immunomodulatory properties. They effectively regulate immune responses by modulating both innate and adaptive immunity. These Exos can inhibit excessive inflammatory responses and promote tissue repair. Moreover, they participate in antigen presentation, which is essential for activating immune responses. The cargo of these Exos, including ligands, proteins, and microRNAs, can suppress T cell activity or enhance the population of immunosuppressive cells to dampen the immune response. By inhibiting lymphocyte proliferation, acting on macrophages, and increasing the population of regulatory T cells, these Exos contribute to maintaining immune and metabolic homeostasis. Furthermore, they can activate immune-related signaling pathways or serve as vehicles to deliver microRNAs and other bioactive substances to target tumor cells, which holds potential for immunotherapy applications. Given the immense therapeutic potential of MSC-derived Exos, this review comprehensively explores their mechanisms of immune regulation and therapeutic applications in areas such as infection control, tumor suppression, and autoimmune disease management. This article aims to provide valuable insights into the mechanisms behind the actions of MSC-derived Exos, offering theoretical references for their future clinical utilization as cell-free drug preparations.

Developing novel cancer therapies that exploit programmed cell death pathways holds promise for advancing cancer treatment. According to a recently published study in Science, copper death (cuproptosis) occurs when intracellular copper is overloaded, triggering aggregation of lipidated mitochondrial proteins and Fe–S cluster proteins. This intriguing phenomenon is triggered by the instability of copper ions. Understanding the molecular mechanisms behind cuproptosis and its associated genes, as identified by Tsvetkov, including ferredoxin 1, lipoic acid synthase, lipoyltransferase 1, dihydrolipid amide dehydrogenase, dihydrolipoamide transacetylase, pyruvate dehydrogenase α1, pyruvate dehydrogenase β, metallothionein, glutaminase, and cyclin-dependent kinase inhibitor 2A, may open new avenues for cancer therapy. Here, we provide a new understanding of the role of copper death and related genes in cancer.

Diagnosis and treatment of chronic osteomyelitis based on nanomaterials

Effectiveness of platelet-rich plasma in the treatment of Achilles tendon disease

Developing novel cancer therapies that exploit programmed cell death pathways holds promise for advancing cancer treatment. According to a recently published study in Science, copper death (cuproptosis) occurs when intracellular copper is overloaded, triggering aggregation of lipidated mitochondrial proteins and Fe–S cluster proteins. This intriguing phenomenon is triggered by the instability of copper ions. Understanding the molecular mechanisms behind cuproptosis and its associated genes, as identified by Tsvetkov, including ferredoxin 1, lipoic acid synthase, lipoyltransferase 1, dihydrolipid amide dehydrogenase, dihydrolipoamide transacetylase, pyruvate dehydrogenase α1, pyruvate dehydrogenase β, metallothionein, glutaminase, and cyclin-dependent kinase inhibitor 2A, may open new avenues for cancer therapy. Here, we provide a new understanding of the role of copper death and related genes in cancer.

Accessory navicular (AN) is a developmental variation of the secondary ossification center of the navicular tuberosity. Ten percent of patients with AN will have pain symptoms that affect walking and life. As the AN changes the position of the posterior tibial tendon insertion, children with AN often have posterior tibial tendon function insufficiency and flexible flat foot. Surgical treatment is often required after failure of conservative treatment. This article reviewed the etiology, clinical manifestations, complications, and treatment methods of AN.