Abstract:
:Acute renal failure (ARF) is a rapid loss of kidney function. The reasons and mechanism by which this occurs has not been clarified so far thus creating obstacles to management of this disease. Presently, the experimental research using the accepted renal ischemia reperfusion injury (I/R injury) model represented for ARF focuses on several possible relevant factors such as reactive oxygen species, no-reflow phenomenon, apoptosis and extensive inflammatory response. The latter is much talked about currently. Some intracellular danger sensing proteins, such as the nucleotide binding domain leucine rich repeats-containing family proteins known as NLRs, adjust the inflammatory response through the formation of a multi-protein complex known as an inflammasome. The most classic family member of this complex is NALP3 confirmed to serve as a contributor to I/R injury. However, how it contributes to the pathology remains obscure. The extensive inflammatory response is considered to be modulated by the mitogen-activated protein kinases (MAPK) signaling pathway. NOD2, another family member of NLR, which shares similar structure with NALP3, indicated that it induced the activation of MAPK in response to a pathogen, thus we assumed that NALP3 performed the harmful process of I/R injury, resulting probably from the activation of the MAPK signaling pathway. If this hypothesis proves to be correct, it might benefit the management of ARF.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Hao JL,Li YF,Li RSdoi
10.1016/j.mehy.2012.12.041subject
Has Abstractpub_date
2013-04-01 00:00:00pages
463-5issue
4eissn
0306-9877issn
1532-2777pii
S0306-9877(13)00030-3journal_volume
80pub_type
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更新日期:2020-09-01 00:00:00
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pub_type: 杂志文章
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