Glioblastoma multiforme (GBM) is characterized by pronounced immune escape and resistance to chemotherapy-induced apoptosis. Preliminary investigations revealed a marked overexpression of gasdermin E (GSDME) in GBM. Notably, cisplatin (CDDP) demonstrated a capacity of inducing pyroptosis by activating caspase-3 to cleave GSDME, coupled with the release of proinflammatory factors, indicating the potential as a viable approach of inducing anti-tumor immune activation. For the effective delivery of CDDP, the CDDP-polyphenol nanocomplexes were prepared, and catalase and copper ions were incorporated to fortify structural integrity, enhance glutathione (GSH) responsiveness, and ameliorate tumor hypoxia. Additionally, BV2 microglial cells were engineered to overexpress programmed death-1 (PD-1), and the membrane is employed for nanocomplex coating, effectively blocking the CDDP-induced upregulation of programmed death ligand 1 (PD-L1). Furthermore, the angiopep-2 peptide was modified to efficiently cross the blood brain barrier and specifically target GBM cells. In vitro analyses confirmed potent cytotoxicity and characteristic induction of pyroptosis. In vivo assays corroborated the enhancement of tumor targeting, culminating in an obvious suppression of tumor proliferation. A notable activation of immune cells was observed within tumors and lymph nodes, indicative of a synergistic effect of chemotherapy and immunotherapy, underscoring its potential as a safe and efficacious therapeutic strategy against GBM.
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http://dx.doi.org/10.1186/s12951-025-03091-w | DOI Listing |
Sci Rep
January 2025
Department of Basic Sciences, Faculty of Dentistry, Universidad de Antioquia U de A, Medellín, 050010, Colombia.
The NLRP3 inflammasome, regulated by TLR4, plays a pivotal role in periodontitis by mediating inflammatory cytokine release and bone loss induced by Porphyromonas gingivalis. Periodontal disease creates a hypoxic environment, favoring anaerobic bacteria survival and exacerbating inflammation. The NLRP3 inflammasome triggers pyroptosis, a programmed cell death that amplifies inflammation and tissue damage.
View Article and Find Full Text PDFJ Nanobiotechnology
January 2025
Department of Pharmacy The Second Xiangya Hospital, Central South University, Changsha, 410011, China.
Glioblastoma multiforme (GBM) is characterized by pronounced immune escape and resistance to chemotherapy-induced apoptosis. Preliminary investigations revealed a marked overexpression of gasdermin E (GSDME) in GBM. Notably, cisplatin (CDDP) demonstrated a capacity of inducing pyroptosis by activating caspase-3 to cleave GSDME, coupled with the release of proinflammatory factors, indicating the potential as a viable approach of inducing anti-tumor immune activation.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Key Laboratory of Prevention and treatment of cardiovascular and cerebrovascular diseases of Ministry of Education, Gannan Medical University, Ganzhou, 341000, China.
Cerebral ischemia-induced pyroptosis contributes to the dissemination of neuroinflammation, and Nod-like receptor protein-3 (NLRP3) inflammasome plays a key role in this process. Previous studies have indicated that Genistein-3'-sodiumsulfonate (GSS) can inhibit neuroinflammation caused by cerebral ischemia, exert cerebroprotective effects, but its specific mechanism has not been comprehensively understood. The aim of this study was to explore the effect of GSS on ischemic stroke-induced cell pyroptosis.
View Article and Find Full Text PDFInflamm Res
January 2025
Department of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC, USA.
Background: Mitochondria generate the adenosine triphosphate (ATP) necessary for eukaryotic cells, serving as their primary energy suppliers, and contribute to host defense by producing reactive oxygen species. In many critical illnesses, including sepsis, major trauma, and heatstroke, the vicious cycle between activated coagulation and inflammation results in tissue hypoxia-induced mitochondrial dysfunction, and impaired mitochondrial function contributes to thromboinflammation and cell death.
Methods: A computer-based online search was performed using the PubMed and Web of Science databases for published articles concerning sepsis, trauma, critical illnesses, cell death, mitochondria, inflammation, coagulopathy, and organ dysfunction.
Ren Fail
December 2025
Department of Nephrology, Shanxi Provincial People's Hospital, The Fifth Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi, China.
Copper is a vital cofactor in various enzymes, plays a pivotal role in maintaining cell homeostasis. When copper metabolism is disordered and mitochondrial dysfunction is impaired, programmed cell death such as apoptosis, paraptosis, pyroptosis, ferroptosis, cuproptosis, autophagy and necroptosis can be induced. In this review, we focus on the metabolic mechanisms of copper.
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