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An inherent inflammatory response of cardiovascular system by activation of toll-like receptors (TLRs) localized in the myocardium can be set off by an increasing amount of damage-associated molecular patterns (DAMPs) in response to ischemic myocardial injury. TLR2, one of pattern recognition receptors (PRRs) interacts with an endogenous molecule initiating non-infectious cardiac inflammation cascade. Remarkably, numerous studies have demonstrated role of TLR2 as an emerging target for cardiac anti-inflammatory therapies.
Given the significance of TLR2, this short review will concentrate on DAMP-initiated TLR2 signaling and will discuss role of TLR2 absence on cardiomyocyte’s cell membrane on downstream cytokine production and cell death in p38 MAPK and Akt-dependent manner. In this short review, potential of TLR2 inhibitors, which contribute to preservation of cardiac function, will be introduced in addition to recent experimental research progress and the involvement of TLR2 in myocardial inflammation to increase the potential of TLR2 as a therapeutic target.