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Fig. 2 | Molecular and Cellular Therapies

Fig. 2

From: Cross talk of the first-line defense TLRs with PI3K/Akt pathway, in preconditioning therapeutic approach

Fig. 2

TLR preconditioning triggers cross activation of both MyD88-dependent and Trif-dependent pathways with PI3K/Akt. TLR3 exclusively, and TLR4 partly signals via Trif-dependent pathway. A proposed mechanism for the TLR4-MyD88-dependent mechanism to protect against cardiac I/R. TLR4 activation by its ligand, leads to MyD88-dependent iNOS induction and increased NO production. NO protects myocardium via sGC- and cGMP/PKG-dependent mechanisms. Trif is not required for the TLR4-NO-mediated cardiac protection. LPS, lipopolysaccharide; iNOS, inducible nitric-oxide synthase; MyD88, myeloid differentiation factor 88; sGC, soluble guanylate cyclase; PKG, protein kinase G; TLR, toll-like receptor; Trif, TIR-domain-containing adaptor protein inducing interferon-β–mediated transcription factor

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Molecular and Cellular Therapies

ISSN: 2052-8426

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