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Self-Cascaded Pyroptosis-STING Initiators for Catalytic Metalloimmunotherapy.
J Am Chem Soc
January 2025
Institute of Functional Nano & Soft Materials (FUNSOM), Jiangsu Key Laboratory for Carbon-Based Functional Materials and Devices, Soochow University, Suzhou 215123, China.
Gasdermin (GSDM)-mediated pyroptosis involves the induction of mitochondrial damage and the subsequent release of mitochondrial DNA (mtDNA), which is anticipated to activate the cGAS-STING pathway, thereby augmenting the antitumor immune response. However, challenges lie in effectively triggering pyroptosis in cancer cells and subsequently enhancing the cGAS-STING activation with specificity. Herein, we developed intelligent self-cascaded pyroptosis-STING initiators of cobalt fluoride (CoF) nanocatalysts for catalytic metalloimmunotherapy.
View Article and Find Full Text PDFPPARα suppresses growth of hepatocellular carcinoma in a high-fat diet context by reducing neutrophil extracellular trap release.
JHEP Rep
January 2025
Department of Hepatobiliary Surgery and Fujian Institute of Hepatobiliary Surgery, Fujian Medical University Union Hospital, Fuzhou, China.
Background & Aims: The role of infiltrating neutrophils in hepatocellular carcinoma (HCC) is modulated by cellular metabolism, specifically lipid homeostasis. Throughout the progression of HCC, alterations in lipid metabolism are intricately linked with regulation of neutrophil function and the release of neutrophil extracellular traps (NETs). However, how much the protumor effect of a high-fat diet (HFD) depends on NETs and the potential interplay between NETs and other leukocytes in HCC remains uncertain.
View Article and Find Full Text PDFInhibition of CCR2 attenuates NLRP3-dependent pyroptosis after myocardial ischaemia-reperfusion in rats via the NF-kB pathway.
Int Immunopharmacol
January 2025
Department of Cardiovascular Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230001, China. Electronic address:
Myocardial infarction (MI) is a leading cause of mortality worldwide, contributing significantly to long-term cardiac dysfunction and heart failure. Effective therapeutic strategies are urgently needed to mitigate the extensive damage caused by MI and subsequent ischemia-reperfusion (I/R) injury. This study investigates the role of the Chemokine receptor 2 (CCR2) in regulating NLRP3-dependent cardiomyocyte pyroptosis following myocardial ischemia-reperfusion (MIR), elucidating its molecular mechanisms.
View Article and Find Full Text PDFPurinergic P2X7 receptor mediates hyperoxia-induced injury in pulmonary microvascular endothelial cells via NLRP3-mediated pyroptotic pathway.
Open Med (Wars)
December 2024
Department of Neonatology, Chengdu Women's and Children's Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, 611731, Sichuan, China.
Background: Hyperoxia-induced injury is a well-recognized cause of bronchopulmonary dysplasia (BPD). Existing research studies have not well elucidated the exact mechanisms underlying hyperoxia-induced cellular damage. This study examines the involvement of the P2X7 receptor (P2X7R) in hyperoxia-induced damage to human pulmonary microvascular endothelial cells (HPMVECs) via the NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) pathway.
View Article and Find Full Text PDFThe Stimulator of Interferon Genes Deficiency Attenuates Diabetic Myopathy Through Inhibiting NLRP3-Mediated Pyroptosis.
J Cachexia Sarcopenia Muscle
February 2025
Department of Nephrology, Center for Regeneration and Aging Medicine, The Fourth Affiliated Hospital of School of Medicine, and International School of Medicine, International Institutes of Medicine, Zhejiang University, Zhejiang-Denmark Joint Laboratory of Regeneration and Aging Medicine, Yiwu, Zhejiang, China.
Background: Diabetic myopathy is characterized by the loss of skeletal muscle mass and function. NOD-like receptor family pyrin domain containing 3 (NLRP3)-mediated pyroptosis is a type of proinflammatory cell death, which can exacerbate significant muscle cell loss and adverse remodelling. The stimulator of interferon genes (STING) is an essential molecule involved in the regulation of inflammation and immune responses across various diseases.
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