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Browsing by Subject "Inflammasomes"
Now showing items 1-6 of 6
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Bladder fibrosis during outlet obstruction is triggered through the NLRP3 inflammasome and the production of IL-1β.
(American journal of physiology. Renal physiology, 2017-09)Bladder outlet obstruction (BOO) triggers inflammation in the bladder through the NLRP3 inflammasome. BOO also activates fibrosis, which is largely responsible for the decompensation of the bladder in the chronic state. ... -
Inflammasomes in the urinary tract: a disease-based review.
(American journal of physiology. Renal physiology, 2016-10)Inflammasomes are supramolecular structures that sense molecular patterns from pathogenic organisms or damaged cells and trigger an innate immune response, most commonly through production of the proinflammatory cytokines ... -
Mitochondrial Quality Control as a Therapeutic Target.
(Pharmacol Rev, 2016-01)In addition to oxidative phosphorylation (OXPHOS), mitochondria perform other functions such as heme biosynthesis and oxygen sensing and mediate calcium homeostasis, cell growth, and cell death. They participate in cell ... -
The Emerging Role of Inflammasomes as Central Mediators in Inflammatory Bladder Pathology.
(Current urology, 2018-02)Irritative voiding symptoms (e.g. increased frequency and urgency) occur in many common pathologic conditions such as urinary tract infections and bladder outlet obstruction, and these conditions are well-established to ... -
The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction.
(The Journal of urology, 2016-05)While bladder outlet obstruction is well established to elicit an inflammatory reaction in the bladder that leads to overactive bladder and fibrosis, little is known about the mechanism by which this is initiated. NLRs (NOD-like ... -
The Yersinia pestis Effector YopM Inhibits Pyrin Inflammasome Activation.
(PLoS pathogens, 2016-12-02)Type III secretion systems (T3SS) are central virulence factors for many pathogenic Gram-negative bacteria, and secreted T3SS effectors can block key aspects of host cell signaling. To counter this, innate immune responses ...