Results 81 to 90 of about 17,938 (260)
Inflammation, Immunity, and Cardiovascular Diseases
Cardiovascular stress signals (e.g., hemodynamic shear, oxidized lipids, and ischemia) act on endothelial and immune cells to activate and amplify inflammation through NF‐κB, the NLRP3 inflammasome, and JAK/STAT signaling, inducing proinflammatory cytokines/chemokines (IL‐6, IL‐1β, TNF‐α, and CCL2) and self‐amplifying circuits; clinically, inflammatory
Dezhi Guo +8 more
wiley +1 more source
Background Necroptosis, a form of programmed cell death mediated by receptor interacting serine/threonine-protein kinase-3 (RIPK3), is implicated in murine models of acute respiratory distress syndrome (ARDS).
Michael G. S. Shashaty +14 more
doaj +1 more source
Poly-ubiquitination in TNFR1-mediated necroptosis [PDF]
Tumor necrosis factor (TNF) is a master pro-inflammatory cytokine, and inappropriate TNF signaling is implicated in the pathology of many inflammatory diseases.
Henning Walczak +3 more
core +3 more sources
Doxorubicin induces cardiac and skeletal muscle atrophy by upregulating E3 ubiquitin ligases, inhibiting myogenic regulatory factors, and activating necroptosis. Cardiac atrophy can further exacerbate cardiotoxicity. 6‐Shogaol negatively regulates these processes and attenuates doxorubicin‐induced cardiac and skeletal muscle atrophy.
Xipeng Sun +5 more
wiley +1 more source
Experimental workflow and main findings of the study. ABSTRACT Visceral pain is a major symptom of inflammatory bowel diseases (IBDs), requiring effective treatment strategies. Gut epithelium, beyond maintaining barrier integrity and microbiota homeostasis, modulates neurosensorial circuitries, influencing visceral sensitivity.
Francesco Margiotta +7 more
wiley +1 more source
Kinase domain dimerization drives RIPK3-dependent necroptosis [PDF]
Necroptotic cell death is promoted by the dimerization-dependent activation of the kinase RIPK3.
Saravanan Raju +8 more
openaire +2 more sources
Mechanisms of TNF-independent RIPK3-mediated cell death
Apoptosis and necroptosis regulate many aspects of organismal biology and are involved in various human diseases. TNF is well known to induce both of these forms of cell death and the underlying mechanisms have been elaborately described. However, cells can also engage apoptosis and necroptosis through TNF-independent mechanisms, involving, for example,
Bart Tummers, Douglas R. Green
openaire +2 more sources
Receptor-Interacting Protein Kinase 3 Deficiency Delays Cutaneous Wound Healing. [PDF]
Wound healing consists of a complex, dynamic and overlapping process involving inflammation, proliferation and tissue remodeling. A better understanding of wound healing process at the molecular level is needed for the development of novel therapeutic ...
Andrew Godwin +6 more
doaj +1 more source
Summary: Receptor-interacting protein kinase 3 executes a form of regulated necrosis called necroptosis. Upon induction of an altered conformation by chemical inhibitors or via mutations in its kinase site, RIPK3 associates with a multiprotein complex ...
Kartik Gupta, Bo Liu
doaj +1 more source
Caspase-8 functions as a key mediator of inflammation and pro-IL-1β processing via both canonical and non-canonical pathways. [PDF]
Caspase-8 is an apical component of cell death pathways. Activated caspase-8 can drive classical caspase-dependent apoptosis and actively inhibits cell death mediated by RIPK3-driven necroptosis.
Bryant, Clare E, Monie, Tom P
core +2 more sources

