Topic: renin-angiotensin system

The renin-angiotensin system (RAS) is expressed in the brain and impacts physiological several activities. Dysregulation of the RAS may be associated with a wide spectrum of brain diseases defined by severe neuroinflammation, oxidative stress, and age-related pathophysiological processes. The CAG-hACE2 transgenic mice were designed to express the human angiotensin-converting enzyme 2 (hACE2) receptor, which is involved in the RAS. However, the relevance of ACE2 at the brain level remains unclear. The purpose of our research is to characterize CAG-hACE2 transgenic mice of both sexes, females an

The heptapeptide angiotensin (Ang 1-7: Asp-Arg-Val-Tyr-Ile-His-Pro) is one of the main endogenous components of the protective arm of the renin-angiotensin system (RAS). Acting on the Mas receptor (MasR), it exhibits vasodilator, antiproliferative, anti-inflammatory, and neuroprotective effects. To improve its enzymatic stability, water solubility, and receptor affinity, some new structural analogs of the natural peptide Ang 1-7 with conformationally constrained amino acids have been synthesized, characterized, and tested for biological activity. Solid-phase peptide synthesis—the Fmoc-strategy

The renin-angiotensin system (RAS) is a key regulator of body homeostasis and is involved in modulating brain functions. Two opposing arms are thought to constitute the RAS: the pressor arm consists of Ang II, and AT1 receptors, mediating vasoconstrictor, proliferative, and proinflammatory effects, and the AT2 receptor, which opposes the effects of the AT1R. The depressor arm includes angiotensin-converting enzyme type 2 (ACE2) and Ang-(1-7), which mediate vasodilatory, antiproliferative, anti-inflammatory, and neuroprotective effects through the Mas receptor (MasR). This study aimed to elucid

Blood-brain barrier (BBB) disruption and the consequent alteration of solute and ion transport play a pivotal role in the onset and progression of many neurological diseases, including epilepsy. Among the players that have been shown to modulate BBB function, our group recently demonstrated that Kv7 channels, a family of voltage-gated potassium channels, are critical modulators of barrier permeability, both in physiological conditions and experimental models of seizures. Accumulating evidence suggest that the renin-angiotensin system (RAS) is altered during epilepsy and affects BBB permeabilit