Neural Regeneration Research最新文献

Myasthenia gravis is a chronic autoimmune disorder that affects the neuromuscular junction leading to fluctuating skeletal muscle fatigability. The majority of myasthenia gravis patients have detectable antibodies in their serum, targeting acetylcholine receptor, muscle-specific kinase, or related proteins. Current treatment for myasthenia gravis involves symptomatic therapy, immunosuppressive drugs such as corticosteroids, azathioprine, and mycophenolate mofetil, and thymectomy, which is primarily indicated in patients with thymoma or thymic hyperplasia. However, this condition continues to pose significant challenges including an unpredictable and variable disease progression, differing response to individual therapies, and substantial long-term side effects associated with standard treatments (including an increased risk of infections, osteoporosis, and diabetes), underscoring the necessity for a more personalized approach to treatment. Furthermore, about fifteen percent of patients, called "refractory myasthenia gravis patients", do not respond adequately to standard therapies. In this context, the introduction of molecular therapies has marked a significant advance in myasthenia gravis management. Advances in understanding myasthenia gravis pathogenesis, especially the role of pathogenic antibodies, have driven the development of these biological drugs, which offer more selective, rapid, and safer alternatives to traditional immunosuppressants. This review aims to provide a comprehensive overview of emerging therapeutic strategies targeting specific immune pathways in myasthenia gravis, with a particular focus on preclinical evidence, therapeutic rationale, and clinical translation of B-cell depletion therapies, neonatal Fc receptor inhibitors, and complement inhibitors.

JOURNAL/nrgr/04.03/01300535-202605000-00037/figure1/v/2025-10-21T121913Z/r/image-tiff Mesenchymal stromal cell transplantation is an effective and promising approach for treating various systemic and diffuse diseases. However, the biological characteristics of transplanted mesenchymal stromal cells in humans remain unclear, including cell viability, distribution, migration, and fate. Conventional cell tracing methods cannot be used in the clinic. The use of superparamagnetic iron oxide nanoparticles as contrast agents allows for the observation of transplanted cells using magnetic resonance imaging. In 2016, the National Medical Products Administration of China approved a new superparamagnetic iron oxide nanoparticle, Ruicun, for use as a contrast agent in clinical trials. In the present study, an acute hemi-transection spinal cord injury model was established in beagle dogs. The injury was then treated by transplantation of Ruicun-labeled mesenchymal stromal cells. The results indicated that Ruicun-labeled mesenchymal stromal cells repaired damaged spinal cord fibers and partially restored neurological function in animals with acute spinal cord injury. T2*-weighted imaging revealed low signal areas on both sides of the injured spinal cord. The results of quantitative susceptibility mapping with ultrashort echo time sequences indicated that Ruicun-labeled mesenchymal stromal cells persisted stably within the injured spinal cord for over 4 weeks. These findings suggest that magnetic resonance imaging has the potential to effectively track the migration of Ruicun-labeled mesenchymal stromal cells and assess their ability to repair spinal cord injury.

Neurodegenerative diseases are prevalent conditions that greatly impact human health. These diseases are primarily characterized by the progressive loss and eventual death of neuronal function, although the precise mechanisms underlying these processes remain incompletely understood. Iron is an essential trace element in the human body, playing a crucial role in various biological processes. The maintenance of iron homeostasis relies on the body's intricate and nuanced regulatory mechanisms. In recent years, considerable attention has been directed toward the relationship between dysregulated iron homeostasis and neurodegenerative diseases. The regulation of iron homeostasis within cells is crucial for maintaining proper nervous system function. Research has already revealed that disruptions in iron homeostasis may lead to ferroptosis and oxidative stress, which, in turn, can impact neuronal health and contribute to the development of neurodegenerative diseases. This article primarily explores the intimate relationship between iron homeostasis and neurodegenerative diseases, aiming to provide novel insights and strategies for treating these debilitating conditions.

The interleukin-17 family is the key group of cytokines and displays a broad spectrum of biological functions, including regulating the inflammatory cascade in various autoimmune and inflammatory diseases, such as multiple sclerosis, neuromyelitis optica spectrum disorder, myasthenia gravis, Guillain-Barre syndrome, acute disseminated encephalomyelitis, diabetes, inflammatory skin diseases, joint inflammation, and cancer. Although the function of the interleukin-17 family has attracted increasing research attention over many years, the expression, function, and regulation mechanisms of different interleukin-17 members are complicated and still only partially understood. Currently, the interleukin-17A pathway is considered a critical therapeutic target for numerous immune and chronic inflammatory diseases, with several monoclonal antibodies against interleukin-17A having been successfully used in clinical practice. Whether other interleukin-17 members have the potential to be targeted in other diseases is still debated. This review first summarizes the recent advancements in understanding the physicochemical properties, physiological functions, cellular origins, and downstream signaling pathways of different members and corresponding receptors of the interleukin-17 family. Subsequently, the function of interleukin-17 in various immune diseases is discussed, and the important role of interleukin-17 in the pathological process of immune diseases is demonstrated from multiple perspectives. Then, the current status of targeted interleukin-17 therapy is summarized, and the effectiveness and safety of targeted interleukin-17 therapy are analyzed. Finally, the clinical application prospects of targeting the interleukin-17 pathway are discussed.