Effect of Aliskiren on Circulating Endothelial Progenitor Cells and Vascular Function in Patients With Type 2 Diabetes and Essential Hypertension

Raptis, Athanasios; Markakis, Konstantinos; Mazioti, Maria; Ikonomidis, Ignatios; Maratou, Eirini; Vlahakos, Dimitrios; Kotsifaki, Eleni; Voumvourakis, Astrinos; Tsirogianni, Alexandra; Lambadiari, Vaia; Lekakis, John; Raptis, Sotirios A.; Dimitriadis, George

doi:10.1093/ajh/hpu119

Cited by 36 publications

(35 citation statements)

References 40 publications

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“…Previous studies have shown that aliskiren can increase the number of EPCs in the context of atherosclerosis in hypercholesterolemic mice [35], and in patients with type 2 diabetes and hypertension [36]. However, the potential role of aliskiren to modulate EPCs in the setting of ischemia-induced neovascularization has not been studied.…”

Section: Discussionmentioning

confidence: 99%

Direct renin inhibition with aliskiren improves ischemia-induced neovascularization: Blood pressure-independent effect

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Direct renin inhibition with aliskiren improves ischemia-induced neovascularization: Blood pressure-independent effect

et al. 2015

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“…The AQUARIUS study, which analyzed the effects of the drug in prehypertensive individuals with coronary atherosclerosis, concluded that it did not offer any additional benefit to patients (Nicholls et al, ). However, many studies reported beneficial effects of ALI in regard to endothelial function and arterial rigidity (Bonadei et al, ; Fukutomi, Hoshide, Mizuno, & Kario, ; Raptis et al, ). Furthermore, it reduces ventricular mass according to the ALLAY study, which revealed that ALI is as effective as losartan in the reduction of hypertrophied ventricular mass in hypertensive patients with BMI >25 kg/m 2 (Solomon et al, ).…”

Section: Discussionmentioning

confidence: 99%

The use of aliskiren as an antifibrotic drug in experimental models: A systematic review

Marin

Bertassoli²,

Carvalho

et al. 2019

Drug Development Research

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Aliskiren is an oral antihypertensive medication that acts by directly inhibiting renin. High levels of circulating renin and prorenin activate the pathological signaling pathway of fibrosis. This drug also reduces oxidative stress. Thus, the aim of this systematic review is to analyze experimental studies that show the actions of aliskiren on fibrosis. PubMed and LILACS databases were consulted using the keywords aliskiren and fibrosis within the period between 2005 and 2017. Fifty‐three articles were analyzed. In the heart, aliskiren attenuated remodeling, hypertrophy, inflammatory cytokines, collagen deposition, and oxidative stress. In the kidneys, there was a reduction in interstitial fibrosis, the infiltration of inflammatory cells, apoptosis, proteinuria, and in the recruitment of macrophages. In diabetic models, an improvement in the albumin/creatinine relationship and in the insulin pathway in skeletal muscles was observed; aliskiren was beneficial to pancreatic function and glucose tolerance. In the liver, aliskiren reduced fibrosis, steatosis, inflammatory cytokines, and collagen deposition. In the lung and peritoneal tissues, there was a reduction in fibrosis. Many studies have reported on the beneficial effects of aliskiren on endothelial function and arterial rigidity. A reduction in fibrosis in different organs is cited by many authors, which complies with the results found in this review. However, studies diverge on the use of the drug in diabetic patients. Aliskiren has antifibrotic potential in several experimental models, interfering with the levels of fibrogenic cytokines and oxidative stress. Therefore, its use in diseases in which fibrosis plays an important pathophysiological role is suggested.

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“…The possible benefits of ALI on other physiological targets, such as endothelial function and arterial stiffness, on which recent studies have suggested favorable effects [108,109,110] warrant further investigation. Also, the exact clinical implications in the role of disease of the (pro)renin receptor and PRA levels should be established, as ALI has an effect on both.…”

Section: Discussionmentioning

confidence: 99%

Renin Inhibition with Aliskiren: A Decade of Clinical Experience

Pantzaris

Karanikolas

Tsiotsios

et al. 2017

JCM

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The renin-angiotensin-aldosterone system (RAAS) plays a key role in the pathophysiology of arterial hypertension as well as in more complex mechanisms of cardiovascular and renal diseases. RAAS-blocking agents like angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers, have long been key components in the treatment of essential hypertension, heart failure, diabetic nephropathy, and chronic kidney disease, showing benefits well beyond blood pressure reduction. Renin blockade as the first step of the RAAS cascade finally became possible in 2007 with the approval of aliskiren, the first orally active direct renin inhibitor available for clinical use and the newest antihypertensive agent on the market. In the last decade, many clinical trials and meta-analyses have been conducted concerning the efficacy and safety of aliskiren in comparison to other antihypertensive agents, as well as the efficacy and potential clinical use of various combinations. Large trials with cardiovascular and renal endpoints attempted to show potential benefits of aliskiren beyond blood pressure lowering, as well as morbidity and mortality outcomes in specific populations such as diabetics, heart failure patients, and post-myocardial infarction individuals. The purpose of this review is to present the currently available data regarding established and future potential clinical uses of aliskiren.

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Effect of Aliskiren on Circulating Endothelial Progenitor Cells and Vascular Function in Patients With Type 2 Diabetes and Essential Hypertension

Abstract: Aliskiren had a favorable effect on endothelial function and EPCs, reduced arterial stiffness, and improved LV twisting and untwisting. These effects were independent of BBP lowering, as they were not observed after the achievement of similar values of BBP with HCTZ.

Cited by 36 publications

References 40 publications

Direct renin inhibition with aliskiren improves ischemia-induced neovascularization: Blood pressure-independent effect

Direct renin inhibition with aliskiren improves ischemia-induced neovascularization: Blood pressure-independent effect

The use of aliskiren as an antifibrotic drug in experimental models: A systematic review

Renin Inhibition with Aliskiren: A Decade of Clinical Experience

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