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Immunotherapy stands as a powerful weapon against tumors. However, tumor cells evade recognition and attack by the immune system through various mechanisms, achieving immune escape and exhibiting resistance to immunotherapy. Metalloimmunotherapy, as an emerging paradigm for immunotherapy, offers the potential to effectively overcome the limitations of current tumor immunotherapies. Nevertheless, developing highly efficient and specific metal-based agents for regulating the tumor immune system remains a significant challenge. The modulation of oxidative stress in the tumor microenvironment (TME) by metals presents novel breakthroughs for metalloimmunotherapy, particularly in enhancing immune responses, optimizing immune cell function, and reprogramming the immunosuppressive TME. Copper, a transition metal closely associated with tumor development, acts as an immune activator to enhance immune responses through oxidative stress. Benefiting from advances in nanomaterials, copper-based nanomedicines have demonstrated significant potential in improving the efficacy of cancer immunotherapy by modulating oxidative stress via Fenton-like reactions and enzymatic catalytic activities. Therefore, summarizing recent advances in copper-based nanomedicine activating tumor immunity through oxidative stress modulation provides new insights and drives progress for metalloimmunology. This review outlines strategies utilizing oxidative stress modulated by copper-based nanomedicines to induce or enhance immunotherapy through multiple forms of regulated cell death (RCD), drug co-delivery approaches, and versatile combination therapies. Finally, we discuss current challenges and offer perspectives on copper-based nanomedicines in tumor immunotherapy. Our review aims to elucidate the potential of copper-based nanomedicines in tumor immunology, providing insights for the future development of tumor immunotherapies based on metal and redox biology.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289571 | PMC |
http://dx.doi.org/10.3389/fphar.2025.1646890 | DOI Listing |
Neurochem Res
September 2025
Biology and Health Laboratory, Faculty of Sciences, Ibn Tofail University, Kenitra, Morocco.
Parkinson's disease (PD) is characterized by impairments in motor control following the degeneration of dopamine-producing neurons located in the substantia nigra pars compacta. Environmental pesticides such as Paraquat (PQ) and Maneb (MB) contribute to the onset of PD by inducing oxidative stress (OS). This study evaluated the therapeutic efficacy of moderate physical activity (PA) on both motor and non-motor symptoms in a Wistar rat model of Paraquat and Maneb (PQ/MB) induced PD.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Behbahan Faculty of Medical Sciences, Behbahan, Iran.
Metab Brain Dis
September 2025
Department of Neuroscience, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Brain ischemia is a major global cause of disability, frequently leading to psychoneurological issues. This study investigates the effects of 4-aminopyridine (4-AP) on anxiety, cognitive impairment, and potential underlying mechanisms in a mouse model of medial prefrontal cortex (mPFC) ischemia. Mice with mPFC ischemia were treated with normal saline (NS) or different doses of 4-AP (250, 500, and 1000 µg/kg) for 14 consecutive days.
View Article and Find Full Text PDFCell Biochem Biophys
September 2025
Faculty of Industrial Sciences and Technology, Universiti Malaysia Pahang Al-Sultan Abdullah, Lebuhraya Persiaran Tun Khalil Yaakob, Gambang, Kuantan, Pahang, Malaysia.
Mol Cell Biochem
September 2025
Peking University Third Hospital, Beijing, China.
Cardiovascular-Kidney-Metabolic (CKM) syndrome, a newly defined systemic disorder, is characterized by the pathological interplay among diabetes, chronic kidney disease (CKD), and cardiovascular disease (CVD). Recent studies have identified chronic inflammation not only as a central mediator in the pathological progression of CKM syndrome but also as a pivotal molecular hub that drives coordinated damage across multiple organ systems. Mechanistic investigations have revealed that aberrant activation of signaling pathways such as NF-κB, Wnt, PI3K-AKT, JAK-STAT, and PPAR constitutes a complex inflammatory regulatory network.
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