Results 81 to 90 of about 17,938 (260)

Inflammation, Immunity, and Cardiovascular Diseases

open access: yesMed Research, EarlyView.
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

Plasma receptor interacting protein kinase-3 levels are associated with acute respiratory distress syndrome in sepsis and trauma: a cohort study

open access: yesCritical Care, 2019
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]

open access: yes, 2016
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

6‐Shogaol Attenuates Doxorubicin‐Induced Cardiac and Skeletal Muscle Atrophy by Inhibiting E3 Ubiquitin Ligases and Necroptosis

open access: yesPhytotherapy Research, EarlyView.
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

A Combined Colon Organoid‐Sensory Neuron Model Reveals Epithelial Contribution to Moringin Efficacy Against Painful Inflammatory Bowel Disease

open access: yesPhytotherapy Research, EarlyView.
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]

open access: yesScience Signaling, 2018
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

open access: yesBiochemical Journal, 2022
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]

open access: yesPLoS ONE, 2015
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

PLK1-mediated S369 phosphorylation of RIPK3 during G2 and M phases enables its ripoptosome incorporation and activity

open access: yesiScience, 2021
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]

open access: yes, 2015
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

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