Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
- Known as:
- Mouse pab CIAS1 _ NALP3, Host Mouse
- Catalog number:
- YF-PA26812
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal CIAS1 _ NALP3 Host
Related genes to: Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
- Gene:
- NLRP3 NIH gene
- Name:
- NLR family pyrin domain containing 3
- Previous symbol:
- C1orf7, CIAS1, DFNA34
- Synonyms:
- AGTAVPRL, AII, AVP, FCAS, FCU, NALP3, PYPAF1, MWS, CLR1.1
- Chromosome:
- 1q44
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2019-04-23
Related products to: Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
Related articles to: Mouse polyclonal to CIAS1 _ NALP3, Host Mouse
- Cerebral ischemia-reperfusion injury (CIRI) worsens outcomes after ischemic stroke, yet effective pharmacological interventions remain limited. Echinocystic acid (EA), a pentacyclic triterpenoid isolated from the fruits of Gleditsia sinensis Lam., has shown neuroprotective activity in CIRI, but its direct molecular target and underlying mechanism remain unclear. In this study, using network pharmacology, molecular docking, surface plasmon resonance, and subsequent validation in middle cerebral artery occlusion (MCAO) mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-treated BV2 cells, we identified peroxisome proliferator-activated receptor γ (PPARγ) as a potential target of EA and provided evidence supporting direct binding between EA and PPARγ. EA significantly reduced infarct volume and brain edema while improving neurological outcomes in MCAO mice, and also attenuated OGD/R-induced injury in BV2 cells. Mechanistically, EA restored PPARγ expression, promoted microglial M2 polarization, reduced IL-1β, IL-6, and TNF-α levels, increased IL-10 production, and attenuated NLRP3/Caspase-1/GSDMD-associated pyroptotic signaling in both in vivo and in vitro models. These effects were largely reversed by the PPARγ antagonist GW9662. Collectively, these findings indicate that EA protects against CIRI, at least in part, through a PPARγ-dependent mechanism involving promotion of microglial M2 polarization and attenuation of NLRP3/Caspase-1/GSDMD-associated pyroptotic signaling, highlighting the therapeutic potential of EA in CIRI. - Source: PubMed
Publication date: 2026/09/11
Zou Yi-KaiZhang HuiLiu Jian-XiaHe Shu-YiYang Jiao-YangPeng Hai-JingZhang Jia-XiSun JingMin Jia-Wei - Post-traumatic stress disorder (PTSD) is associated with persistent dysregulation of cellular stress pathways and altered neuronal signaling within limbic and prefrontal circuits. Increasing evidence indicates that activation of endoplasmic reticulum stress responses, oxidative imbalance, and inflammasome signaling contribute to sustained neurobiological alterations underlying PTSD symptomatology. Stress-induced activation of inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6 (ATF6) interacts with inflammatory mediators such as interleukin-18 (IL-18) and interleukin-1β (IL-1β), amplifying neuroimmune responses. Activation of the NOD-like receptor family pyrin domain containing 3 inflammasome (NLRP3 inflammasome) and caspase-1 promotes cytokine maturation and microglial activation, leading to impaired synaptic plasticity. These mechanisms are accompanied by alterations in glutamatergic and gammaaminobutyric acid (GABA) signaling, oxidative stress imbalance, and dysregulation of the hypothalamic-pituitary-adrenal axis. Neuroimaging data demonstrate volumetric and microstructural changes in the hippocampus, amygdala, and prefrontal cortex in chronic PTSD, suggesting structural correlates of prolonged inflammatory and stress-related activity. Biomarker studies further indicate associations between inflammatory mediators, coping strategies, sleep disturbances, and illness duration. These findings support the concept that increased cellular stress responses and altered neuronal signaling are central components of PTSDpathophysiology rather than secondary epiphenomena. Understanding the interaction between endoplasmic reticulum stress, inflammasome activation, oxidative imbalance, and neurotransmitter dysregulation may improve biomarker-based diagnostics and facilitate development of targeted therapeutic interventions. - Source: PubMed
Ogłodek Ewa Alicja - Myocardial injury is a common pathological endpoint in conditions such as acute myocardial infarction, ischemia/reperfusion injury, myocarditis, and drug-induced cardiotoxicity, and remains a therapeutic challenge due to the irreversible loss of cardiomyocytes and subsequent ventricular remodeling. Current strategies lack effective interventions directly targeting regulated cell death pathways. This review centers on the dysregulation of the regulated cell death (RCD) and autophagic network. We comprehensively integrate the dual roles, and evidence-graded crosstalk among RCD modalities (apoptosis, pyroptosis, and ferroptosis) and autophagic responses, proposing a paradigm shift from isolated pathway inhibition to dynamic rebalancing of the RCD and autophagic network for cardioprotection. Within this framework, we consolidate and compare evidence illustrating how active metabolites, single botanical drugs, and compound formulations of traditional Chinese medicine regulate multiple forms of RCD-associated signaling and autophagic processes. The multi-metabolite, multi-target nature enables coordinated regulation at the cellular survival-death checkpoint. Mechanistically, TCM interventions can: (1) attenuate apoptotic marker expression and context-dependently modulate autophagic responses via axes such as PI3K/Akt/mTOR, AMPK/mTOR, MAPK, and JAK/STAT; (2) suppress NLRP3/caspase-1/GSDMD-mediated pyroptotic signaling markers; and (3) modulate lipid peroxidation-associated ferroptotic signaling through antioxidant pathways centered on the Nrf2/GPX4 and System x axes. These actions collectively ameliorate upstream pathological loops involving oxidative stress, inflammatory amplification, and mitochondrial dysfunction. This review adopts a comprehensive cardiovascular toxicology perspective to integrate the regulatory mechanisms of RCD and autophagic networks in myocardial injury, encompassing both exogenous drug-induced cardiotoxicity (e.g., doxorubicin) and endogenous toxic stresses, including lipotoxicity, ROS-mediated toxicity, and ischemia-related metabolic injury. Notably, many TCM agents exhibit cross-RCD and autophagic synergistic effects supported by direct perturbation-and-rescue evidence (Level c crosstalk) as well as co-regulatory profiles, suggesting that cardioprotection at the network level may be achieved through shared hub nodes. This perspective provides a clearer mechanistic landscape for elucidating the action of TCM formulas and for screening novel therapeutic candidates. Ultimately, it advocates for advancing traditional Chinese medicine-based myocardial protection strategies into reproducible, quantifiable, and clinically verifiable pharmacological research systems oriented around RCD and autophagic network homeostasis. - Source: PubMed
Publication date: 2026/09/11
Dong SiyiYan GuangliLiu HuiqiangSun HuiLin ChuanKong LingWang Xijun - Although extensive evidence links chronic pain to an increased cardiovascular risk, its direct impact on myocardial ischemia-reperfusion (MI/R) remains poorly understood. In mice, chronic pain was induced using chronic constriction injury (CCI) of the brachial plexus. We found that chronic pain significantly increased myocardial infarction area, endothelial cell apoptosis and inflammation, accompanied by the increase in sympathetic nerve tone around the endothelial cells. Viral tracer results demonstrated the existence of anatomical connections between the SCG and the heart. The results of c-Fos staining and heart rate variability monitoring indicated that the SCG-cardiac circuit was excessive activated. Chemical sympathectomy of SCG using 6-hydroxydopamine (6-OHDA) effectively alleviated myocardial injury, endothelial cell apoptosis and inflammation. Additionally, the NLRP3 inflammasome of endothelial cells was upregulated in mice with chronic pain. Both ablation of SCG and MCC950 inhibited NLRP3 expression and alleviate myocardial infarction area, endothelial cell apoptosis and inflammation. Finally, bisoprolol not only reduced heart rate, but also decreased myocardial infarction, inhibited endothelial cell apoptosis and NLRP3 expression. In conclusion, sympathetic nerve-driven endothelial apoptosis and inflammation were key pathological processes through which chronic pain exacerbated MI/R injury. The sympathetic-NLRP3 pathway contributed at least in part to the phenotype, with endothelial cells as an important but not exclusive target. Although the current data were obtained exclusively from young male mice, these findings establish a conserved mechanistic framework that warrants validation in female, aged, and clinically relevant models. - Source: PubMed
Publication date: 2026/09/11
Tian MiZhuang ChengruiHe JianHe WanyouWang HanbingWu Fancan - Rare diseases (RDs) are individually uncommon but collectively affect a large global population, and the vast majority still lack effective disease-modifying therapies. With advances in genomics and data-sharing platforms, research has increasingly shifted from a single-disease perspective to the search for convergent molecular pathways that might be shared across clinically distinct entities. In this context, the purinergic P2X7 receptor (P2X7R) has emerged as a putative "shared molecular platform" due to its central role in inflammation amplification, cell death and immune regulation. P2X7R is an ATP-gated ion channel with unique structural and functional features: under high extracellular ATP, it not only forms a non-selective cation channel but can also dilate into a "large pore" permeable to macromolecules, thereby triggering Caoverload, NLRP3 inflammasome assembly, reactive oxygen species (ROS) production and apoptotic/necrotic-like cell death. This review briefly outlines the epidemiology of RDs and the structural-functional characteristics of P2X7R, then systematically summarizes current evidence linking P2X7R to multiple rare diseases, including Charcot-Marie-Tooth disease, Guillain-Barré syndrome, amyotrophic lateral sclerosis, Huntington's disease, multiple sclerosis, and selected inflammatory and metabolic RDs (CAPS, familial Mediterranean fever, Systemic sclerosis, Dravet syndrome and Gaucher disease). By comparing P2X7R expression and functional alterations, downstream signaling pathways and pharmacological data from animal models across these conditions, we propose that a P2X7R-dependent network centered on a "Ca-NLRP3-inflammation/cell death axis" may constitute a common pathogenic backbone for diverse RDs. At the same time, disease-specific spatiotemporal expression patterns of P2X7R in central vs peripheral nervous systems and in immune vs target organ cells confer marked context dependence and "double-edged sword" properties. Finally, we discuss opportunities and challenges for P2X7R-targeted strategies, including the impact of disease stage and sex differences on therapeutic efficacy, and key bottlenecks in translating preclinical findings into clinical benefit. A deeper understanding of both shared and disease-specific roles of P2X7R may provide a conceptual framework and therapeutic entry point for precision stratification and multi-target interventions in rare diseases. - Source: PubMed
Publication date: 2026/09/05
Xiao XinyiCao GegeHou ShuaiYin Haiyan