IMMUNE MODULATION AND ApTOLL
After a stroke, cell damage induced by the lack of blood supply causes the release of endogenous cell components to the neuron extracellular medium, triggering central nervous system alarms. One of the primary sensors of these brain damage-associated molecular patterns (DAMPs) is TLR4, a central receptor in innate immunity and expressed on the plasmatic membrane of immune cells such as microglia, neutrophils, monocytes, macrophages, among others. TLR4’s activation initiates a cascade of triggers that ultimately leads to the production and release of pro-inflammatory mediators, causing uncontrolled inflammation, further cell damage, and subsequent worsening of the brain lesion. ApTOLL has a powerful immunomodulatory effect through antagonistic action on TLR4 receptors, inhibiting the inflammatory cascade.
Scientific publications
Beneficial effect of TLR4 blockade by a specific aptamer antagonist after acute myocardial infarction
Biomedicine & Pharmacotherapy (2023)
Targeting TLR4 with ApTOLL Improves Heart Function in Response to Coronary Ischemia Reperfusion in Pigs Undergoing Acute Myocardial Infarction
Biomolecules (2020)
Toll-like receptor 4 is involved in brain damage and inflammation after experimental stroke
Circulation (2007)
I am text block. Click edit button to change this text. Lorem ipsum dolor sit amet, consectetur adipiscing elit. Ut elit tellus, luctus nec ullamcorper mattis, pulvinar dapibus leo.