Inflammopharmacology, Journal Year: 2024, Volume and Issue: unknown
Published: Dec. 17, 2024
Language: Английский
Inflammopharmacology, Journal Year: 2024, Volume and Issue: unknown
Published: Dec. 17, 2024
Language: Английский
Neurochemical Research, Journal Year: 2025, Volume and Issue: 50(2)
Published: Jan. 30, 2025
Language: Английский
Citations
1Neurochemistry International, Journal Year: 2025, Volume and Issue: 184, P. 105950 - 105950
Published: Feb. 18, 2025
Language: Английский
Citations
1International Immunopharmacology, Journal Year: 2024, Volume and Issue: 139, P. 112739 - 112739
Published: July 28, 2024
Language: Английский
Citations
4Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 12, 2025
Language: Английский
Citations
0European Journal of Pharmacology, Journal Year: 2025, Volume and Issue: 993, P. 177385 - 177385
Published: Feb. 14, 2025
Language: Английский
Citations
0Biochimica 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
0Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: April 1, 2025
Spinal cord ischemia-reperfusion injury (SCIRI) leads to severe neurological deficits, with pyroptosis emerging as a key driver of inflammation and neuronal death. Recent studies suggest that methyltransferase-like 3 (METTL3), critical RNA methyltransferase, may regulate the nucleotide-binding oligomerized structural domain-like receptor protein (NLRP3) inflammasome activation via N6-Methyladenosine (m6A) modification, yet direct evidence in SCIRI remains limited. This review synthesizes current knowledge on METTL3-NLRP3 axis pyroptosis, explores its therapeutic potential, identifies research gaps for future investigation.
Language: Английский
Citations
0CNS Neuroscience & Therapeutics, Journal Year: 2025, Volume and Issue: 31(3)
Published: March 1, 2025
ABSTRACT Aims Spinal cord ischemia–reperfusion injury (SCIRI) is a disastrous complication that cannot be completely prevented in thoracoabdominal aneurysm surgery, leading to sensory and motor dysfunction even paraparesis, causing tremendous socioeconomic burden. Ferritinophagy form of autophagic ferroptosis, which contributor SCIRI. Hydrogen sulfide (H 2 S) has been reported neuroprotective various diseases. However, it remains unclear whether H S alleviates SCIRI‐induced neural death via regulating ferritinophagy‐mediated ferroptosis. The aim this study was explore their relationship interaction Results results demonstrate Nissl bodies function were obviously lost SCIRI rats. Meanwhile, led significant increase DHE‐positive neurons, TUNEL‐positive LC3‐positive ferritin‐positive downregulation GPx4, Slc7a11, p62, ferritin expression, upregulation LC3 II/I NCOA4 expression. Additionally, there the level MDA, GSH, Fe 2+ . Finally, we found could significantly relieve neuronal loss rats by inhibiting ferritinophagy Conclusion Ferroptosis play crucial role etiopathogenesis SCIRI, exerts neuroprotection
Language: Английский
Citations
0Neurobiology of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 106907 - 106907
Published: April 1, 2025
PANoptosis represents a highly coordinated inflammatory programmed cell death governed by the assembly and activation of PANoptosome, which strategically integrate core molecular elements from pyroptosis, apoptosis, necroptosis. The triple-component pathways set themselves apart alternative regulated mechanisms through their unique capacity to concurrently process signals derived multiple death-signaling modalities, thereby coordinating multifaceted cellular defense system against diverse pathological insults. Pathogen-associated patterns synergistically interact with cytokine storms, oncogenic stress active PANoptosis, establishing this pathway as critical nexus in pathogenesis tumor immunomodulation. This crosstalk highlights promising therapeutic target for managing immune-related disorders malignant transformation. Emerging evidence links neuroinflammatory dysregulated between (apoptosis, necroptosis, pyroptosis) accidental necrosis, driving neuronal loss neural damage. Single-cell transcriptomics reveals spatially resolved signatures Alzheimer's hippocampal microenvironments sclerosis demyelinating plaques, distinct clusters correlating quantifiable metrics. PANoptosis-targeted therapies show preclinical promise alleviating neurovascular dysfunction while preserving physiological microglial surveillance functions. Accumulating linking (particularly PANoptosis) neurological underscores urgency deciphering its developing precision modulators next-generation therapies. review systematically deciphers PANoptosome associated cascades, evaluates roles multiscale regulatory networks, proposes frameworks advance neurology.
Language: Английский
Citations
0Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)
Published: May 2, 2025
Language: Английский
Citations
0