RT Journal Article
T1 AT1 receptor autoantibodies mediate effects of metabolic syndrome on dopaminergic vulnerability
A1 Pedrosa Sánchez, María Ángeles
A1 Labandeira Guerra, Carmen María
A1 Valenzuela Limiñana, Rita
A1 Quijano Ocampo, Aloia
A1 Sánchez Andrade, Mariña
A1 Suárez Quintanilla, Juan
A1 Lanciego Pérez, José Luis
A1 Labandeira García, José Luis
A1 Rodríguez Pérez, Ana Isabel
K1 Autoimmunity
K1 ACE2
K1 Blood–brain-barrier
K1 Diabetes
K1 27-Hydroxycholesterol
K1 Hypertension
K1 Obesity
K1 Neurodegeneration
K1 Parkinson
K1 Renin-angiotensin system
AB The metabolic syndrome has been associated to chronic peripheral inflammation and related with neuroinflammation and neurodegeneration, including Parkinson’s disease. However, the responsible mechanisms are unclear. Previous studies have involved the brain renin-angiotensin system in progression of Parkinson’s disease and the angiotensin receptor type 1 (AT1) has been recently revealed as a major marker of dopaminergic vulnerability in humans. Dysregulation of tissue renin-angiotensin system is a key common mechanism for all major components of metabolic syndrome. Circulating AT1 agonistic autoantibodies have been observed in several inflammation-related peripheral processes, and activation of AT1 receptors of endothelial cells, dopaminergic neurons and glial cells have been observed to disrupt endothelial blood -brain barrier and induce neurodegeneration, respectively. Using a rat model, we observed that metabolic syndrome induces overactivity of nigral pro-inflammatory renin-angiotensin system axis, leading to increase in oxidative stress and neuroinflammation and enhancing dopaminergic neurodegeneration, which was inhibited by treatment with AT1 receptor blockers (ARBs)
PB Elsevier
YR 2022
FD 2022
LK http://hdl.handle.net/10347/29904
UL http://hdl.handle.net/10347/29904
LA eng
NO Brain, Behavior, and Immunity 108 (2023). https://doi.org/10.1016/j.bbi.2022.12.009
DS Minerva
RD 24 abr 2026