Identification of cross-talk pathways and PANoptosis-related genes in periodontitis and Alzheimer’s disease by bioinformatics analysis and machine learning DOI Creative Commons
Xiantao Chen, Yifei Dai, Y.-F. Li

et al.

Frontiers in Aging Neuroscience, Journal Year: 2024, Volume and Issue: 16

Published: Aug. 27, 2024

Background and objectives Periodontitis (PD), a chronic inflammatory disease, is serious threat to oral health one of the risk factors for Alzheimer’s disease (AD). A growing body evidence suggests that two diseases are closely related. However, current studies have not provided comprehensive understanding common genes mechanisms between PD AD. This study aimed screen crosstalk AD potential relationship cross-talk PANoptosis-related genes. The core immune cells will be analyzed provide new targets clinical treatment. Materials methods datasets were downloaded from GEO database differential expression analysis was performed obtain DEGs. Overlapping DEGs had linking OP, obtained literature review. Pearson coefficients used compute gene correlations in datasets. Cross-talk intersection AD-related genes, protein-protein interaction(PPI) networks constructed identified using STRING database. defined as cross-talk-PANoptosis Core screened ROC XGBoost. PPI subnetwork, gene-biological process, gene-pathway based on In addition, infiltration CIBERSORT algorithm. Results 366 overlapping with 109 XGBoost showed MLKL, DCN, IL1B, IL18 more accurate than other predicting well better overall characterization. GO KEGG analyses four involved immunity inflammation organism. Immune B naive, Plasma cells, T gamma delta significantly differentially expressed patients compared normal group. Finally, 10 drugs associated retrieved DGIDB Conclusion reveals joint mechanism PANoptosis. Analyzing may therapeutic directions pathogenesis combined

Language: Английский

PANoptosis in intestinal epithelium: its significance in inflammatory bowel disease and a potential novel therapeutic target for natural products DOI Creative Commons

Chuanxiang Zhao,

Shan Lin

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 7, 2025

The intestinal epithelium, beyond its role in absorption and digestion, serves as a critical protective mechanical barrier that delineates the luminal contents gut microbiota from lamina propria within resident mucosal immune cells to maintain homeostasis. is manifested contiguous monolayer of specialized epithelial (IEC), interconnected through tight junctions (TJs). integrity this paramount. Consequently, excessive IEC death advances permeability consequence thereof translocation bacteria into propria, subsequently triggering an inflammatory response, which underpins clinical disease trajectory bowel (IBD). A burgeoning body evidence illustrates landscape where undergoes several model programmed cell (PCD) pathophysiology pathogenesis IBD. Apoptosis, necroptosis, pyroptosis represent principal modalities PCD with intricate specific pathways molecules. Ample has revealed substantial mechanistic convergence crosstalk among these three aforementioned forms death, expanding conceptualization PANoptosis orchestrated by PNAoptosome complex. This review provides concise overview molecular mechanisms apoptosis, pyroptosis. Furthermore, based on between deaths IEC, details current knowledge regarding regulation natural products. Our objective broaden comprehension innovative underlying IBD furnish foundation for developing more drugs treatment IBD, benefiting both practitioners research workers.

Language: Английский

Citations

3
Z-DNA binding protein 1 orchestrates innate immunity and inflammatory cell death DOI
Qixiang Song, Yuhang Fan, Huali Zhang

et al.

Cytokine & Growth Factor Reviews, Journal Year: 2024, Volume and Issue: 77, P. 15 - 29

Published: March 26, 2024

Language: Английский

Citations

11
Regulated Cell death in Acute Myocardial Infarction: Molecular Mechanisms and Therapeutic Implications DOI
Lili Zhu,

Yiyang Liu,

Kangkai Wang

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 104, P. 102629 - 102629

Published: Dec. 5, 2024

Language: Английский

Citations

5
A novel approach to the prevention and management of chemotherapy-induced cardiotoxicity: PANoptosis DOI Creative Commons
Chenchen Meng,

Yali Wang,

Tiantian Zheng

et al.

Chemico-Biological Interactions, Journal Year: 2025, Volume and Issue: 407, P. 111379 - 111379

Published: Jan. 8, 2025

Language: Английский

Citations

0
Shank3 forms a complex with Gal-3 and ZBP-1 to alleviate PANoptosis in TIA of female ovariectomized mice DOI Creative Commons
Lei Zhang,

Yaowen Luo,

Jimeng Zhang

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 3, 2025

Abstract Selective neuron death or loss, which induced by specific pathogen- and damage-associated molecular patterns (PAMPs DAMPs), was the main reason results in high morbidity, disability, mortality of transient ischemic attack (TIA) man postmenopausal women. Shank3, a key postsynaptic density, is correlated with synaptic dysfunction, oxidative stress, inflammatory, apoptosis poor outcomes stroke, although its role menopausal women TIA remains elusive. Here we discovered that Shank3 direct binds Gal-3, positive regulator aging inflammation, then regulates innate immune sensors ZBP-1, to drive inflammatory signaling cell death, PANoptosis, during TIA. Base on defeminization models (a stable female mouse OVX + model first established as well an vitro cultured primary desexualization tOGD/R model), blockade amplify stress arouse persistent behavioral deficits infarction formation, does not appear de-estrogen combination damage mice. We also observed Gal-3 ZBP-1 were members large multi-protein complex along Caspase 3, 7, 8, 9, 1, NLRP GSDMD, GSDME, RIPK 3 MLKL drove neuronal-special PANoptosis. In addition, administration natural inhibitor, D-allose, used for food sweetener, produces anti-PANoptosis effects via activating but inhibiting ZBP-1. Collectively, our findings establish previously unknown regulatory connection interaction among driver neuron-specific PANoptosis TIA, reveal activate such as, maybe potential strategy halt neuronal loss

Language: Английский

Citations

0
Inhibition of Piezo1 Ameliorates Septic Cardiomyopathy by Blocking Calcium-Dependent PANoptosis DOI

Yanting Zhang,

Hui‐Hua Li, Fei Teng

et al.

European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 177438 - 177438

Published: Feb. 1, 2025

Language: Английский

Citations

0
Ischemia-reperfusion injury induces ZBP1-dependent PANoptosis in endothelial cells DOI
Yue Cui,

Lin Huang,

Jiaxing Ma

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 167782 - 167782

Published: March 1, 2025

Language: Английский

Citations

0
Fucoxanthin from Laminaria japonica Targeting PANoptosis and Ferroptosis Pathways: Insights into Its Therapeutic Potential Against Ovarian Cancer DOI Creative Commons

Yaze Wang,

Yimin Mao,

Hui Liu

et al.

Marine Drugs, Journal Year: 2025, Volume and Issue: 23(3), P. 123 - 123

Published: March 12, 2025

Ovarian cancer (OC) is a highly aggressive malignancy with poor prognosis, necessitating novel therapeutic strategies. Fucoxanthin (FX), marine-derived carotenoid from Laminaria japonica, has demonstrated promising anticancer potential. This study revealed that FX exerts multiple effects in OC by inhibiting cell proliferation, invasion, and migration, while inducing various forms of programmed death (PCD). triggered PANoptosis (apoptosis, necroptosis, pyroptosis) ferroptosis. treatment regulated key markers associated PANoptosis, including apoptosis (Bcl-2, cleaved caspase-3), pyroptosis (GSDME), necroptosis (RIPK3). Additionally, modulated ferroptosis-related markers, such as SLC7A11 GPX4, increasing reactive oxygen species (ROS) Fe2+ levels disrupting mitochondrial function. Proteomic molecular docking analyses identified AMP-activated protein kinase (AMPK) direct target, activating the AMPK/Nrf2/HMOX1 pathway to promote In vivo, significantly reduced tumor growth xenograft models, accompanied enhanced ferroptosis marker expression. These findings demonstrate induces through promotes via distinct mechanisms, highlighting its potential agent for OC.

Language: Английский

Citations

0
Design of a Highly Active Peptide Inhibitor of Farnesyltransferase and Its Protective Effect Against Acute Liver Failure DOI Creative Commons
Chun-Lian Huang, Hui Qu, Anne Li

et al.

Drug Design Development and Therapy, Journal Year: 2025, Volume and Issue: Volume 19, P. 1909 - 1926

Published: March 1, 2025

Acute liver failure (ALF) is a fatal syndrome associated with massive hepatocyte death. Previous studies have found that Farnesyltransferase (FTase) inhibitors improve disease progression in mouse models of endotoxemia, sepsis, and autoimmune hepatitis. PANoptosis novel type programmed cell death (PCD), including pyroptosis, apoptosis, necrosis, plays an important role ALF. This study was designed investigated whether the FTase inhibitor PD083176 (d2,d3,d5) could attenuate ALF by modulating PANoptosis. Combining technical tools computational biology, structural biology pharmacology, we obtained three high-affinity human PD083176(d2,d3,d5). Then, these were animal experiments administering PD083176(d2,d3,d5) (10 mg/kg) before modeling LPS (100 μg/kg)/D-GalN (300 or TAA (800 mg/kg). We induced LPS/D-GaIN increased farnesylated protein liver. not only inhibited hepatic proteins but also significantly attenuated injury mortality mice. Importantly, treatment effectively apoptosis (Bax, Bcl-xL TUNEL counts), pyroptosis (Caspase-1 GSDMD), necrotic (RIPK1 RIPK3). Collectively, findings demonstrate PD081376(d2,d3,d5) alleviate TAA-induced regulating necrotizing which might provide new therapeutic strategy scalability challenge for

Language: Английский

Citations

0
Cell death in acute lung injury: caspase-regulated apoptosis, pyroptosis, necroptosis, and PANoptosis DOI Creative Commons
Jun Xiao,

Lichuan Wang,

Bohan Zhang

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 21, 2025

There has been abundant research on the variety of programmed cell death pathways. Apoptosis, pyroptosis, and necroptosis under action caspase family are essential for innate immune response. Caspases classified into inflammatory caspase-1/4/5/11, apoptotic caspase-3/6/7, caspase-2/8/9/10. Although is not caspase-dependent to transmit signals, it can cross-link with pyroptosis apoptosis signals regulation caspase-8. An increasing number studies have reiterated involvement in acute lung injuries caused by bacterial viral infections, blood transfusion, ventilation, which influenced noxious stimuli that activate or inhibit engagement pathways, leading subsequent injury. This article reviews role caspases implicated diverse mechanisms injury status relevant inhibitors against target proteins described mechanisms. The findings this review may help delineating novel therapeutic targets

Language: Английский

Citations

0