Purpose Of Review: Vasculitis are a group of heterogeneous conditions characterized by chronic inflammation of blood vessels, leading to tissue destruction and organ failure. Vasculitis is an inflammatory process in which immune effector cells infiltrate blood vessels and surrounding tissues. The involvement of inflammasomes seems to occur during inflammatory processes.
Recent Findings: Studies have emphasized that genetic susceptibility is an important aspect of the pathogenesis of vasculitis. The innate immune system is a major contributor to these inflammatory diseases, suggesting that the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome plays a key role. NLRP3 activation causes the assembly of a large multiprotein and leads to the secretion of bioactive interleukin (IL)-1β and IL-18 as well as the induction of inflammatory cell death, termed pyroptosis. Accumulating evidence confirms the involvement of this cascade in sterile inflammatory diseases and other vascular diseases.
Summary: In this review, we will summarize the current state of knowledge regarding the role of NLRP3 inflammasome in vascular diseases, and discuss the potential of the NLRP3 inflammasome as a therapeutic target.
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http://dx.doi.org/10.1097/BOR.0000000000000962 | DOI Listing |
Neurosurg Rev
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Department of Critical Care Medicine, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Zhou shan hui shui Community,199 Hailing South Road, Taizhou, Jiangsu Province, 225300, China.
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View Article and Find Full Text PDFJ Nanobiotechnology
January 2025
Department of Orthopedic Surgery, Fujian Medical University Union Hospital, Fuzhou, 350001, China.
Overproduction of reactive oxygen species (ROS), elevated synovial inflammation, synovial hyperplasia and fibrosis are the main characteristic of microenvironment in rheumatoid arthritis (RA). Macrophages and fibroblast-like synoviocytes (FLSs) play crucial roles in the progression of RA. Hence, synergistic combination of ROS scavenging, macrophage polarization from pro-inflammatory M1 phenotype towards M2 anti-inflammatory phenotype, and restoring homeostasis of FLSs will provide a promising therapeutic strategy for RA.
View Article and Find Full Text PDFJ Neurotrauma
January 2025
Department of Neurosurgery, the First Medical Centre, Chinese PLA General Hospital, Beijing, China.
Following traumatic brain injury (TBI), inhibition of the Na-K-Cl cotransporter1 (NKCC1) has been observed to alleviate damage to the blood-brain barrier (BBB). However, the underlying mechanism for this effect remains unclear. This study aimed to investigate the mechanisms by which inhibiting the NKCC1 attenuates disruption of BBB integrity in TBI.
View Article and Find Full Text PDFImmunity
January 2025
Institute for Stroke and Dementia Research (ISD), University Hospital, Ludwig-Maximilian-University (LMU), Munich, Germany; Deutsches Zentrum für Neurodegenerative Erkrankungen e. V. (DZNE), Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance (MHA), Munich, Germany. Electronic address:
Common genetic variants in a conserved cis-regulatory element (CRE) at histone deacetylase (HDAC)9 are a major risk factor for cardiovascular disease, including stroke and coronary artery disease. Given the consistency of this association and its proinflammatory properties, we examined the mechanisms whereby HDAC9 regulates vascular inflammation. HDAC9 bound and mediated deacetylation of NLRP3 in the NACHT and LRR domains leading to inflammasome activation and lytic cell death.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
School of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Microglia-mediated neuroinflammation plays a crucial role in Alzheimer's disease (AD). Tinosinenside A (Tis A) is a novel sesquiterpene glycoside isolated from the dried rattan stem of Tinospora sinensis (Lour.) Merr.
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