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ABSTRACT: Background
Increased levels of monocytic angiotensin-converting enzyme (ACE) found in haemodialysis (HD) patients may directly participate in the pathogenesis of atherosclerosis. We demonstrated recently that uremia triggers the development of highly pro-atherogenic monocytes via an angiotensin II (AngII)–dependent mechanism. Opposing actions of the AngII-degrading ACE2 remain largely unknown. We examined the status of both ACEs and related receptors in circulating leukocytes of HD, not-dialyzed CKD and healthy individuals. Furthermore, we tested the possible impact of monocytic ACEs on atherogenesis and behaviour of the cells under conditions mimicking chronic renal failure.Methods
Expression of ACE, ACE2, AT1R, AT2R and MASR was investigated on circulating leukocytes from
SUBMITTER: Trojanowicz B
PROVIDER: S-EPMC7108029 | biostudies-literature | 2017 Feb
REPOSITORIES: biostudies-literature