Tight control of the severity, duration and location of inflammation is an absolute requirement for an appropriate balance between clearance of injured tissue and pathogens versus damage to host cells.

Potential therapeutic targets involved in provoking the inflammation include Toll-like receptors (TLRs) and their downstream signaling molecules responsible for their critical role in various chronic inflammatory diseases.

Signaling pathways via TLR4 activate various transcription factors like NF-κB, AP1, STAT1, and IRFs. Inhibition of these targets and their upstream signaling molecules provide a potential therapeutic approach to treat inflammatory diseases.

In this article, we have highlighted the already known inflammatory signaling players and discussed about the recent advancements in discovery of potential targets within the major TLR-4 mediated pathway.

SiR4 activs like nuclear factor kappa-light-chain-enhancer (NF-κB), activator protein 1 (AP1), signal transducers and activators of tran(STAT1) and nterferon regulatory factors (IRF's),