The vagus nerve can limit inflammation via the α7 nicotinic acetylcholine receptor
(α7nAChR). Selective pharmacological stimulation of the α7nAChR may have therapeutic …

Macrophages/monocytes and the proinflammatory mediators, such as tumour necrosis factor
(TNF)-α, prostaglandin E2 (PGE2), macrophage inflammatory protein (MIP)-1α and MIP-1α …

Previous reports have indicated that artificial stimulation of the vagus nerve reduces
systemic inflammation in experimental models of sepsis. This phenomenon is a part of a …

Excessive activation of pro‐inflammatory M1 macrophages following acute myocardial
infarction (MI) aggravates adverse cardiac remodelling and heart dysfunction. There are two …

The cholinergic antiinflammatory pathway favorably influences end organ damage induced
by inflammatory conditions. Here, we hypothesized that α7 and/or α4β2-nicotinic …

Activation of nicotinic acetylcholine receptors (nAChRs) expressed by innate immune cells
can attenuate pro-inflammatory responses. Silent nAChR agonists, which down-modulate …

Rationale: This study was performed to gain insights into novel therapeutic approaches for
the treatment of autoimmune myocarditis. Objective: Chemical stimulation of the efferent arm …

The α7 nicotinic acetylcholine receptor (α7-nAChR) is associated with inflammation, re-
epithelialization, and angiogenesis in wound healing process. A recent study demonstrated …

Immune cell infiltration in response to myocyte death regulates extracellular matrix
remodeling and scar formation after myocardial infarction (MI). Caspase-recruitment domain …

Background Myocardial infarction (MI) reperfusion therapy causes paradoxical cardiac
complications. Following restoration of blood flow to infarcted regions, a multitude of …