Biglycan-triggered TLR-2- and TLR-4-signaling exacerbates the pathophysiology of ischemic acute kidney injury
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- 作者：Kristin Moretha ; 1 ; Helena Freya ; Mario Huboa ; Jinyang Zeng-Brouwersa ; Madalina-Viviana Nastasea ; Louise Tzung-Harn Hsieha ; Riad Hacenia ; Josef Pfeilschiftera ; Renato V. Iozzob ; Liliana Schaefera ; schaefer@med.uni-frankfurt.de" class="auth_mail
- 关键词：CCL ; chemokine (C&ndash ; C motif) ligand ; CCR2 ; C&ndash ; C chemokine receptor type 2 ; CXCL ; neutrophil chemoattractant chemokine C&ndash ; X&ndash ; C motif ligand ; IL-1尾 ; interleukin-1尾 ; IRI ; ischemia&ndash ; reperfusion injury ; LPS ; lipopolysaccharide ; NF-魏B ; nuclear factor kappa-light-chain enhancer of activated B cells ; NLRP3 ; NLR family ; pyrin domain-containing 3 ; PGN ; peptidoglycan ; SEAP ; secreted alkaline phosphatase ; TLR ; Toll-like receptor
- 刊名：Matrix Biology
- 出版年：April 2014
- 年：2014
- 卷：35
- 期：Complete
- 页码：143-151
- 全文大小：1190 K
文摘
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Renal ischemia–reperfusion injury (IRI) elevates biglycan in plasma and kidney.
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Soluble biglycan directly interacts with TLR-2 and TLR-4.
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Overexpression of soluble biglycan worsens pathophysiology of renal IRI.
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Disabled biglycan-triggered TLR-2/TLR-4 signaling in renal IRI is renoprotective.