Role of the CCL5 and Its Receptor, CCR5, in the Genesis of Aldosterone-Induced Hypertension, Vascular Dysfunction, and End-Organ Damage.
Rafael M CostaDébora M CerqueiraAriane Bruder-NascimentoJuliano V AlvesWanessa Mayumi Carvalho AwataShubhnita SinghAlexander KufnerDouglas Silva PradoEbin JohnyEugenia Cifuentes-PaganoWilliam F HawsePartha DuttaPatrick J PaganoJacqueline HoThiago Bruder-NascimentoPublished in: Hypertension (Dallas, Tex. : 1979) (2024)
Our data demonstrate that CCL5/CCR5, through activation of NFκB and NOX1, is critically involved in aldosterone-induced vascular and renal damage and hypertension placing CCL5 and CCR5 as potential therapeutic targets for conditions characterized by aldosterone excess.
Keyphrases
- oxidative stress
- liver injury
- drug induced
- diabetic rats
- blood pressure
- dendritic cells
- high glucose
- angiotensin ii
- liver fibrosis
- regulatory t cells
- signaling pathway
- electronic health record
- endothelial cells
- machine learning
- lps induced
- risk assessment
- big data
- reactive oxygen species
- artificial intelligence
- cell proliferation
- toll like receptor
- binding protein
- deep learning