Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.abb.2019.07.001 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Angiogenesis, a key point in the association of gut microbiota and its metabolites with disease.
Eur J Med Res
December 2024
Department of Gastrointestinal Surgery, Shandong Provincial Hospital, Shandong University, Jinan, 250021, Shandong, China.
The gut microbiota is a complex and dynamic ecosystem that plays a crucial role in human health and disease, including obesity, diabetes, cardiovascular diseases, neurodegenerative diseases, inflammatory bowel disease, and cancer. Chronic inflammation is a common feature of these diseases and is closely related to angiogenesis (the process of forming new blood vessels), which is often dysregulated in pathological conditions. Inflammation potentially acts as a central mediator.
View Article and Find Full Text PDFExtinguishing the flames of inflammation: retardant effect of chlorquinaldol on NLRP3-driven diseases.
Mol Med
December 2024
TCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Article Synopsis
- - The study explores the potential of chlorquinaldol (CQ), an antimicrobial agent, as a specific inhibitor of the NLRP3 inflammasome, which is linked to various inflammatory diseases, highlighting its promise for drug repurposing.
- - CQ effectively suppresses NLRP3 inflammasome activation in both mouse and human macrophages primarily by blocking the interaction between NLRP3 and ASC, while having minimal impact on other inflammasomes like NLRC4 and AIM2.
- - In vivo tests showed that CQ significantly improves conditions in mouse models of LPS-induced peritonitis, DSS-induced colitis, and MSU-induced gouty arthritis, suggesting its therapeutic potential for treating NLRP3-related
Butyrate attenuates SA-AKI by inhibiting pyroptosis via the STING-GSDMD axis.
Biochem Biophys Res Commun
January 2025
Department of Urology, The First People's Hospital of Zunyi (The Third Affiliated Hospital of Zunyi Medical University), 563000, Zunyi, China; Scientific Research Center, The First People's Hospital of Zunyi (The Third Affiliated Hospital of Zunyi Medical University), 563000, Zunyi, Guizhou, China. Electronic address:
Sepsis-associated acute kidney injury (SA-AKI) is a common and serious complication with high morbidity and mortality. The pathophysiology of SA-AKI is complex. The underlying mechanisms of SA-AKI remain unclear, and effective therapeutic strategies are limited.
View Article and Find Full Text PDFZinc homeostasis regulates caspase activity and inflammasome activation.
PLoS Pathog
December 2024
Key Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, School of Life Sciences, Peking University, Beijing, China.
Inflammasome activation drives pyroptotic cell death and the release of inflammatory cytokines, and many diseases involve its overactivation. Zinc is essential for all organisms as a trace element, but its functions in innate immunity remain undefined. Here, we reported that Zn2+ inhibits caspase-1 to hinder inflammasome activation.
View Article and Find Full Text PDFMETTL4-Mediated Mitochondrial DNA N6-Methyldeoxyadenosine Promoting Macrophage Inflammation and Atherosclerosis.
Circulation
December 2024
Key Laboratory of Cardiovascular and Cerebrovascular Medicine, Nanjing Medical University, China. (L.Z., X.C., X.H., Y.T., J.M., Xinyu Li, H.W., M.C., Y.Z., M.D., Q.Y., D.H., H.J., Xuesong Li, H.C.).
Background: Mitochondrial dysfunction is a key factor in the development of atherogenesis. METTL4 (methyltransferase-like protein 4) mediates N6- methyldeoxyadenosine (6mA) of mammalian mitochondrial DNA (mtDNA). However, the role of METTL4-mediated mitoepigenetic regulation in atherosclerosis is still unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!