Increased Accumulation of Tissue ACE in Human Atherosclerotic Coronary Artery Disease

Abstract

These observations demonstrate that significant sources of tissue ACE in human atherosclerotic plaques are regions of inflammatory cells, especially areas of clustered macrophages as well as microvessel endothelial cells. These results suggest that ACE accumulation within the plaque may contribute to an increased production of local angiotensin that may participate in the pathobiology of coronary artery disease. Plaque ACE probably is an important target of drug action.

Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonist attenuate tumor growth via polarization of neutrophils toward an antitumor phenotype

“…[20][21][22] We hypothesized this mobile RAS might be responsible for the effect of captopril on neutrophil hypersegmentation. To identify RAS components in human neutrophils, the presence of ACE in human neutrophils was examined by reverse transcription polymerase chain reaction (RT-PCR).…”

“…20 Alveolar macrophages express ACE and produce Ang II in human atherosclerotic plaques. 21 Circulating rat leukocytes are also reported to secrete angiotensinogen, 22 and human mononuclear leukocytes possess functional components of RAS that can generate Ang II locally. 30,31 These studies suggest that a mobile RAS present on leukocytes contributes to circulating Ang II levels.…”

Susceptibility to T Cell-Mediated Injury in Immune Complex Disease Is Linked to Local Activation of Renin-Angiotensin System: The Role of NF-AT Pathway

“…In fact, significant sources of tissue ACE in human atherosclerotic plaques are regions of clustered macrophages (56). In addition, IL-12, a key cytokine for Th1 response, from mononuclear cells is suppressed by ACE inhibitors (57).…”

Modulating atherosclerosis through inhibition or blockade of angiotensin

“…33 Tissue ACE has been shown to accumulate in atherosclerotic human coronary arteries as well as in luminal endothelial cells and inflammatory cells, especially in regions of clustered macrophages and T lymphocytes, possibly contributing to increased production of local angiotensin. 34 …”