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JNK Pathway Could Be Implicated in Development of IC/BPS

Zhao J, Wang L, Dong X, Hu X, Zhou L, Liu Q, Song B, Wu Q, Li L. The c-Jun N-terminal kinase (JNK) pathway is activated in human interstitial cystitis (IC) and rat protamine sulfate induced cystitis. Sci Rep. 2016 Feb 17;6:19670. doi: 10.1038/srep19670.

While nobody is quite sure what causes interstitial cystitis/bladder pain syndrome (IC/BPS), many believe that inflammation plays an important role in the disorder. Signaling in a pathway known as JNK has been implicated in a variety of chronic diseases that have an inflammatory component. Thus, scientists have wondered about the role of JNK in IC/BPS, but the amount of research looking at this topic is very limited. To provide more data, this group of investigators looked at the JNK signaling pathway in a rat model of cystitis as well as bladder tissue from human IC/BPS patients. They found that the JNK signaling pathway was indeed activated and resulted in inflammation in the human bladder tissue. Interestingly, they tried treatment with an experimental JNK inhibiting agent called SP600125 and found that it effectively inhibited the expression of markers of the JNK pathway, exerting a protective effect against cystitis in the rats. Based on these findings, the investigators believe that one day, JNK inhibiting agents could be used as a potential treatment option for patients with IC/BPS

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