Life Sciences, Journal Year: 2024, Volume and Issue: unknown, P. 123241 - 123241
Published: Nov. 1, 2024
Language: Английский
Advances in Clinical Medicine, Journal Year: 2025, Volume and Issue: 15(03), P. 2490 - 2504
Published: Jan. 1, 2025
Language: Английский
Citations
0
Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)
Published: April 16, 2025
Language: Английский
Citations
0
International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3747 - 3747
Published: April 16, 2025
Psoriasis, a chronic immune-mediated inflammatory skin disorder characterized by keratinocyte hyperproliferation and cell infiltration, involves multiple distinct programmed death pathways in its pathogenesis. Following the Nomenclature Committee on Cell Death recommendations, we analyzed current literature examining diverse modes of cellular psoriatic lesions, with particular focus patterns their molecular signatures. Analysis revealed several mechanisms: autophagy dysfunction through IL-17A pathways, decreased apoptotic activity lesional skin, medication targeting anoikis psoriasis, upregulated necroptosis mediated RIPK1/MLKL signaling, gasdermin-mediated pyroptosis enhanced IL-1β secretion, coordinated PANoptotic activation specialized complexes, PARP1-mediated parthanatos promoting cutaneous inflammation, iron-dependent ferroptosis correlating Th22/Th17 responses, copper-dependent cuproptosis elevated MTF1/ATP7B/SLC31A1 expression, NETosis amplifying immune responses interaction Th17 axis. The intricate interplay between these mechanisms has led to development targeted therapeutic strategies, including mTOR inhibitors for modulation, RIPK1 necroptosis, various approaches NETosis, providing new directions more effective psoriasis treatments.
Language: Английский
Citations
0
Cellular & Molecular Biology Letters, Journal Year: 2024, Volume and Issue: 29(1)
Published: May 31, 2024
Abstract Background Senecavirus A (SVA) caused porcine idiopathic vesicular disease (PIVD) showing worldwide spread with economic losses in swine industry. Although some progress has been made on host factors regulating the replication of SVA, role Z-DNA binding protein 1 (ZBP1) remains unclear. Methods The expression ZBP1 SVA-infected 3D/421 cells was analyzed by quantitative real-time PCR (qRT-PCR) and western blot. Western blot qRT-PCR were used to detect effects over interference SVA VP2 gene protein. Viral growth curves prepared measure viral proliferation. effect type I interferons (IFNs), interferon-stimulated genes (ISGs), pro-inflammatory cytokines infection qRT-PCR. analysis NF-κB signaling pathway inhibitor are confirm. Results is shown inhibit enhancing mediated antiviral response. significantly up-regulated 3D4/21 cells. Infection overexpression showed that inhibited enhanced IFNs (IFN-α, IFN-β), ISGs (ISG15, PKR, IFIT1) (IL-6, IL-8, TNF-α), while, infected-cells opposite effects. Further results achieved activation specific also confirmed this. Conclusions an important factor indicates may be a novel target against SVA. Graphical
Language: Английский
Citations
3
Viruses, Journal Year: 2024, Volume and Issue: 16(8), P. 1272 - 1272
Published: Aug. 9, 2024
Viruses are obligate intracellular pathogens as their replication depends on the metabolism of host cell. The induction cellular suicide, known programmed cell death (PCD), has potential to hinder viral and act a first line defense against pathogens. Apoptosis, necroptosis, pyroptosis three important PCD modalities. Different signaling pathways involved in execution, they also differ ability cause inflammation. Cytomegaloviruses (CMV), beta-herpesviruses with large double-stranded DNA genomes, encode great variety immune evasion genes, including several suppressors. While CMV inhibitors apoptosis necroptosis have been studied for years, inhibitor identified characterized only recently. Here, we describe how human murine interfere apoptosis, pathways. We discuss importance different forms containment spread vivo.
Language: Английский
Citations
3
Diabetology & Metabolic Syndrome, Journal Year: 2024, Volume and Issue: 16(1)
Published: July 3, 2024
Abstract Background Nonalcoholic fatty pancreatitis (NAFP) presents a pressing challenge within the domain of metabolic disorders, necessitating further exploration to unveil its molecular intricacies and discover effective treatments. Our focus was delve into potential therapeutic impact ZBiotic , specially engineered strain probiotic B. subtilis in managing NAFP by targeting specific genes linked with necroptosis TNF signaling pathway, including TNF, ZBP1, HSPA1B, MAPK3, along their upstream epigenetic regulator, miR-5192, identified through bioinformatics. Methods Rats were subjected either standard or high-fat, high-sucrose diet (HFHS) for eight weeks. Subsequently, they divided groups: model, two additional groups receiving daily doses (0.5 ml 1 ml/kg), original group (1 ml/kg) four weeks, alongside HFHS diet. Results exhibited remarkable efficacy modulating gene expression, leading downregulation miR-5192 target mRNAs ( p < 0.001). Treatment resulted reversal fibrosis, inflammation, insulin resistance, evidenced reductions body weight, serum amylase, lipase levels 0.001), decreased percentages Caspase Nuclear Factor Kappa-positive cells pancreatic sections 0.01). Notably, high-dose displayed superior compared strain, highlighting mitigating progression regulating pivotal genes. Conclusion holds promise curbing advancement, fibrosis inflammation while alleviating pathological irregularities observed animal model. This intricately modulation necroptosis/TNF-mediated pathway-related signatures.
Language: Английский
Citations
2
Aquaculture International, Journal Year: 2024, Volume and Issue: unknown
Published: June 13, 2024
Language: Английский
Citations
1
Life Sciences, Journal Year: 2024, Volume and Issue: unknown, P. 123241 - 123241
Published: Nov. 1, 2024
Language: Английский
Citations
1