Inflammation, coagulation, and cellular injury in heat-induced shock
ConclusionsMultiple mechanisms are involved in the pathogenesis of heat-induced shock. In addition to dehydration, heat stress-induced cardiomyopathy due to the thermal damage of mitochondria, upregulated inflammation via damage-associated molecular patterns released from oncotic cells, unbalanced coagulation/fibrinolysis, and endothelial damage are the major factors that are related to circulatory shock. (Source: Inflammation Research)
Source: Inflammation Research - January 7, 2023 Category: Research Source Type: research
Role of α-synuclein in microglia: autophagy and phagocytosis balance neuroinflammation in Parkinson’s disease
ConclusionIn this review, we discuss the interaction between microglia and α-syn in PD pathogenesis and the possible mechanism of microglial autophagy and phagocytosis in α-syn clearance and inhibition of neuroinflammation. This may provide a novel insight into treatment of PD. (Source: Inflammation Research)
Source: Inflammation Research - January 4, 2023 Category: Research Source Type: research
m6A-related bioinformatics analysis and functional characterization reveals that METTL3-mediated NPC1L1 mRNA hypermethylation facilitates progression of atherosclerosis via inactivation of the MAPK pathway
ConclusionMETTL3-mediated NPC1L1 mRNA hypermethylation facilitates AS progression by regulating the MAPK pathway, and NPC1L1 may be a novel target for the treatment of AS. (Source: Inflammation Research)
Source: Inflammation Research - December 30, 2022 Category: Research Source Type: research
New frontiers in inflammation: from translational research to clinic (information about the 15th World Congress on Inflammation (WCI2022))
AbstractThe following provides a summary of the 15th World Congress on Inflammation (WCI2022), which took place in Rome (Italy) from June 5 to 8, 2022. Presented are the main trends and most promising research developments in the field of inflammation, including identification of cellular and molecular mechanisms and investigation of new pathogenetic pathways, target molecules, genetic mechanisms, and new therapeutic strategies. In addition, described are the primary areas of research engaged in by leading scientific groups and national societies from various countries in the field of inflammatory pathology mechanisms. (So...
Source: Inflammation Research - December 26, 2022 Category: Research Source Type: research
ADAM10-a “multitasker” in sepsis: focus on its posttranslational target
ConclusionsIn this review, we focus on the functions of ADAM10 in sepsis-related complex endothelium-immune cell interactions and microcirculation dysfunction through the diversity of its substrates and its enzymatic activity. In addition, we highlight the posttranslational mechanisms of ADAM10 at specific subcellular sites, or in multimolecular complexes, which will provide the insight to intervene in the pathophysiological process of sepsis caused by ADAM10 dysregulation. (Source: Inflammation Research)
Source: Inflammation Research - December 24, 2022 Category: Research Source Type: research
Loss of pleckstrin homology domain and leucine-rich repeat protein phosphatase 2 has protective effects on high glucose-injured retinal ganglion cells via the effect on the Akt –GSK–3β–Nrf2 pathway
ConclusionsThe loss of PHLPP2 was beneficial for HG-injured RGCs through the effect on the Akt –GSK–3β–Nrf2 pathway. This work suggests a possible role of PHLPP2 in diabetic retinopathy. (Source: Inflammation Research)
Source: Inflammation Research - December 23, 2022 Category: Research Source Type: research
Periostin regulation and cartilage degradation early after anterior cruciate ligament reconstruction
ConclusionPro-inflammatory pathways and periostin were upregulated after ACLR. Periostin demonstrated strong network connections with markers of collagen breakdown, and future work is needed to determine whether periostin may offer a biomarker of early cartilage degradation after ACLR and/or play an active role in early post-traumatic osteoarthritis (PTOA) progression. (Source: Inflammation Research)
Source: Inflammation Research - December 23, 2022 Category: Research Source Type: research
Tissue-resident immune cells in the pathogenesis of multiple sclerosis
AbstractBackgroundMultiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) in which genetic and environmental factors contribute to disease progression. Both innate and adaptive immune cells, including T cells, B cells, activated macrophages and microglia, have been identified to be involved in the pathogenesis of MS, leading to the CNS inflammation, neurodegeneration and demyelination. In recent years, there has been considerable progress in understanding the contribution of tissue-resident immune cells in the pathogenesis of MS.MethodsWe performed a keyword-based search in ...
Source: Inflammation Research - December 22, 2022 Category: Research Source Type: research
Annexin A1 (Ac2-26)-dependent Fpr2 receptor alleviates sepsis-induced acute kidney injury by inhibiting inflammation and apoptosis in vivo and in vitro
ConclusionsTaken together, this study provides evidence that the protective effect of ANXA1 (Ac2-26) on SI-AKI largely depends on the negative regulation of inflammation and apoptosis via the Fpr2 receptor. (Source: Inflammation Research)
Source: Inflammation Research - December 22, 2022 Category: Research Source Type: research
SARS-CoV-2-mediated liver injury: pathophysiology and mechanisms of disease
ConclusionSARS-CoV-2-induced liver inflammation is a serious condition, and drugs with potent anti-inflammatory effect can play a major role in preventing irreversible liver damage in COVID-19. (Source: Inflammation Research)
Source: Inflammation Research - December 20, 2022 Category: Research Source Type: research
Mitophagy-promoting miR-138-5p promoter demethylation inhibits pyroptosis in sepsis-associated acute lung injury
ConclusionsIn summary, our study indicated that mitophagy induced the demethylation of the miR-138-5p promoter, which may subsequently inhibit NLRP3 inflammasome, AM pyroptosis and inflammation in sepsis-induced lung injury. These findings may provide a promising therapeutic target for sepsis-associated ALI. (Source: Inflammation Research)
Source: Inflammation Research - December 20, 2022 Category: Research Source Type: research
The star target in SLE: IL-17
ConclusionIL-17 has a very high potential for the development as a star target in SLE. (Source: Inflammation Research)
Source: Inflammation Research - December 20, 2022 Category: Research Source Type: research
Molecular mechanisms of ferroptosis and relevance to inflammation
ConclusionIn this review, we summarize the regulatory mechanisms associated with ferroptosis, discuss the interaction between ferroptosis and inflammation, the role of mitochondria in inflammatory ferroptosis, and the role of targeting ferroptosis in inflammatory diseases. As more and more studies have confirmed the relationship between ferroptosis and inflammation in a wide range of organ damage and degeneration, drug induction and inhibition of ferroptosis has great potential in the treatment of immune and inflammatory diseases. (Source: Inflammation Research)
Source: Inflammation Research - December 19, 2022 Category: Research Source Type: research
Apolipoprotein D modulates lipid mediators and osteopontin in an anti-inflammatory direction
Conclusion
ApoD is an anti-inflammatory apolipoprotein, which modulates lipid mediators and osteopontin in an anti-inflammatory direction. (Source: Inflammation Research)
Source: Inflammation Research - December 19, 2022 Category: Research Source Type: research
Staphylococcal protein A modulates inflammation by inducing interferon signaling in human nasal epithelial cells
ConclusionSpA induces interferon signaling through activation of the IFNGR1-JAK-2 pathway, which provides an understanding of howS. aureus SpA affects the inflammatory process in the upper airways. (Source: Inflammation Research)
Source: Inflammation Research - December 17, 2022 Category: Research Source Type: research
