2012
DOI: 10.1016/j.urology.2011.09.049
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Increased Cell Apoptosis of Urothelium Mediated by Inflammation in Interstitial Cystitis/Painful Bladder Syndrome

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Cited by 97 publications
(111 citation statements)
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References 29 publications
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“…P38 mitogen-activated protein kinase might be an important mediator of the antiproliferative factor in the bladder urothelial cells [23]. Increased levels of the apoptotic signaling molecules, including Bax, cleaved caspase-3, and Bad were elevated in the IC/BPS bladder tissues [24]. The apoptosis in IC/BPS bladders might be due to upregulation of inflammatory signals.…”
Section: Chronic Inflammation and Apoptosismentioning
confidence: 99%
“…P38 mitogen-activated protein kinase might be an important mediator of the antiproliferative factor in the bladder urothelial cells [23]. Increased levels of the apoptotic signaling molecules, including Bax, cleaved caspase-3, and Bad were elevated in the IC/BPS bladder tissues [24]. The apoptosis in IC/BPS bladders might be due to upregulation of inflammatory signals.…”
Section: Chronic Inflammation and Apoptosismentioning
confidence: 99%
“…We found that BPS/IC was significantly associated with previous statin use, and the Although there is no consensus on a mechanism to explain the underlying cause of BPS/IC, several pathophysiologic mechanisms have been proposed, including epithelial dysfunction, mast cell activation, and neurogenic inflammation [19][20][21] . In addition, many recent studies reported that a higher level of cell apoptosis in the urothelium was associated with inflammation in patients with BPS/IC [22][23][24][25] . We proposed 3 possible explanations for the association between statin use and BPS/IC detected in this study.…”
Section: Discussionmentioning
confidence: 99%
“…Tryptase and tumor necrosis factor a induced endothelial expression of intracellular adhesion molecules, suggesting mast cells play an important role in blood vessel permeability and glomerulations in patients with IC/BPS. 18,19 In preliminary studies, we found that the angiogenesis marker interleukin-8 and VEGF were suppressed under onabotulinumtoxinA therapy. 20 According to our preliminary results (protein array and western blotting), we found that the degree of glomerulations and angiogenic factors could be reduced because of the inflammatory suppression by repeated onabotulinumtoxinA injections in some patients with IC/BPS.…”
Section: Commentmentioning
confidence: 98%
“…19 Moreover, the molecular mechanism of apoptosis in IC/BPS bladders was tumor necrosis factor-a and p38 MAPK mediated. p38 MAPK is a protein kinase that coordinates the cellular responses to many types of stresses, including those that trigger oxidative stress.…”
Section: Commentmentioning
confidence: 99%