MyD88 and Trif Signaling Play Distinct Roles in Cardiac Dysfunction and Mortality during Endotoxin Shock and Polymicrobial Sepsis | Zendy

Yan Feng | Zendy; Lin Zou | Zendy; Ming Zhang | Zendy; Yan Li | Zendy; Chan Chen | Zendy; Wei Chao | Zendy

Open Access

MyD88 and Trif Signaling Play Distinct Roles in Cardiac Dysfunction and Mortality during Endotoxin Shock and Polymicrobial Sepsis

Author(s) -

Yan Feng,

Lin Zou,

Ming Zhang,

Yan Li,

Chan Chen,

Wei Chao

Publication year - 2011

Publication title -

anesthesiology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.874

H-Index - 234

eISSN - 1528-1175

pISSN - 0003-3022

DOI - 10.1097/aln.0b013e31822a22f7

Subject(s) - trif , medicine , sepsis , septic shock , tlr4 , ligation , tlr2 , immunology , cecum , receptor , toll like receptor , inflammation , innate immune system

Toll-like receptors (TLRs) such as TLR2, TLR4, and TLR9 contribute to the pathogenesis of polymicrobial sepsis. These TLRs signal via the common myeloid differentiation factor 88 (MyD88)-dependent pathways. TLR4 also signals through MyD88-independent but TIR domain-containing adaptor inducing interferon-β-mediated transcription factor (Trif)-dependent pathway. The role of the two signaling pathways in cardiac dysfunction during polymicrobial sepsis and endotoxin shock is unknown.

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