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Merck
  • Activation of NLRP3 inflammasomes contributes to hyperhomocysteinemia-aggravated inflammation and atherosclerosis in apoE-deficient mice.

Activation of NLRP3 inflammasomes contributes to hyperhomocysteinemia-aggravated inflammation and atherosclerosis in apoE-deficient mice.

Laboratory investigation; a journal of technical methods and pathology (2017-04-11)
Renqing Wang, Yiqin Wang, Nana Mu, Xiaoying Lou, Weixuan Li, Yanming Chen, Dong Fan, Hongmei Tan
RESUMEN

Hyperhomocysteinemia (HHcy) has been shown to promote vascular inflammation and atherosclerosis, but the underlying mechanisms remain largely unknown. The NLRP3 inflammasome has been identified as the cellular machinery responsible for activation of inflammatory processes. In this study, we hypothesized that the activation of NLRP3 inflammasomes contributes to HHcy-induced inflammation and atherosclerosis. ApoE

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Sigma-Aldrich
Amyloid Protein Non-Aβ Component, ≥80% (HPLC)
Sigma-Aldrich
MISSION® esiRNA, targeting human NLRP3