Detailed Information on Publication Record
2020
The potential actions of angiotensin-converting enzyme II (ACE2) activator diminazene aceturate (DIZE) in various diseases
QARADAKHI, T., L. K. GADANEC, K. R. MCSWEENEY, A. TACEY, V. APOSTOLOPOULOS et. al.Basic information
Original name
The potential actions of angiotensin-converting enzyme II (ACE2) activator diminazene aceturate (DIZE) in various diseases
Authors
QARADAKHI, T. (36 Australia), L. K. GADANEC (36 Australia), K. R. MCSWEENEY (36 Australia), A. TACEY (36 Australia), V. APOSTOLOPOULOS (36 Australia), I. LEVINGER (36 Australia), K. RIMAROVA (703 Slovakia), E. E. EGOM (124 Canada), L. RODRIGO (724 Spain), Peter KRUŽLIAK (703 Slovakia, guarantor, belonging to the institution), P. KUBATKA (703 Slovakia) and A. ZULLI (36 Australia)
Edition
Clinical and Experimental Pharmacology and Physiology, Australia, Blackwell Publishing Australia, 2020, 0305-1870
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30105 Physiology
Country of publisher
United States of America
Confidentiality degree
není předmětem státního či obchodního tajemství
References:
Impact factor
Impact factor: 2.557
RIV identification code
RIV/00216224:14110/20:00115986
Organization unit
Faculty of Medicine
UT WoS
000509618900001
Keywords in English
angiotensin-converting enzyme II; cardiovascular disease; diminazene aceturate; endothelial dysfunction; renin angiotensin system
Tags
International impact, Reviewed
Změněno: 15/7/2020 10:04, Mgr. Tereza Miškechová
Abstract
V originále
The renin angiotensin system (RAS) regulates fluid balance, blood pressure and maintains vascular tone. The potent vasoconstrictor angiotensin II (Ang II) produced by angiotensin-converting enzyme (ACE) comprises the classical RAS. The non-classical RAS involves the conversion of Ang II via ACE2 into the vasodilator Ang (1-7) to counterbalance the effects of Ang II. Furthermore, ACE2 converts AngA into another vasodilator named alamandine. The over activation of the classical RAS (increased vasoconstriction) and depletion of the non-classical RAS (decreased vasodilation) results in vascular dysfunction. Vascular dysfunction is the leading cause of atherosclerosis and cardiovascular disease (CVD). Additionally, local RAS is expressed in various tissues and regulates cellular functions. RAS dysregulation is involved in other several diseases such as inflammation, renal dysfunction and even cancer growth. An approach in restoring vascular dysfunction and other pathological diseases is to either increase the activity of ACE2 or reduce the effect of the classical RAS by counterbalancing Ang II effects. The antitrypanosomal agent, diminazene aceturate (DIZE), is one approach in activating ACE2. DIZE has been shown to exert beneficial effects in CVD experimental models of hypertension, myocardial infarction, type 1 diabetes and atherosclerosis. Thus, this review focuses on DIZE and its effect in several tissues such as blood vessels, cardiac, renal, immune and cancer cells.