The Role of Angiotensin-II in the Cardiovascular System: From Molecular Mechanism to Therapeutic Perspectives
A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".
Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 1254
Special Issue Editor
Special Issue Information
Dear Colleagues,
Ang II (angiotensin II), the main product of the renin–angiotensin system, produces hypertension by activating group IV cPLA2α (cytosolic phospholipase A2α), resulting in arachidonic acid (AA) release and the generation predominantly of eicosanoids with prohypertensive effects. The eicosanoids produced by COX (cyclooxygenase) and PGE2 (prostaglandin E2) by acting on EP1 and EP3, and TXA2 (thromboxane A2) by acting on its TP (prostanoid receptor), contribute to the hypertensive effect of Ang II. Also, AA metabolites generated via 12/15-lipoxygenase and cytochrome P450 A1, 12Sand 20-hydroxy eicosatetraenoic acids, respectively, participate in the vasoconstrictor effect of Ang II and contribute to its prohypertensive effect. There is sexual dimorphism in blood pressure (BP) levels in humans and various animal models of hypertension, attributed to gonadal hormones and sex chromosomes affecting renin–angiotensin and immune cell activity. Ang II produces a more significant pressure effect in men than women. In addition, Ang II infusion produces a higher increase in BP in males than in female animals. Ovariectomy enhances this effect in female mice, and castration reduces the effect of Ang II in male mice to increase BP. However, whether the protection against AngII–induced hypertension in females depends on alteration in the activity of the cPLA2α/AA system is unknown. E2 (17β-estradiol)- CYP1B1-generated metabolite 2-hydroxy estradiol, using its subsequent metabolism via catechol-O-methyltransferase to 2-ME (2-methoxyestradiol), protected against AngII–induced hypertension in female mice. However, the mechanism by which 2-ME protects against AngII–induced hypertension is not known. cPLA2α gene disruption in females, as in male mice, also prevents Ang II-induced hypertension, and thus led to the following hypothesis: CYP1B1-E2-generated metabolite 2-ME acts upstream by inhibiting cPLA2α activity and reducing the generation of prohypertensive. Therefore, eicosanoids protect against AngII–induced hypertension and its pathogenesis.
We cordially invite authors and investigators to submit their original research or review articles related to this Special Issue, “The Role of Angiotensin-II in the Cardiovascular System: From Molecular Mechanism to Therapeutic Perspectives”. This serves as an exceptional opportunity for all investigators to share their knowledge in Angiotensin II–Induced Hypertension research.
Dr. Shubha Ranjan Dutta
Guest Editor
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Keywords
- renin–angiotensin system
- inflammation
- eicosanoids
- arachidonic acid
- cytosolic phospholipase A2α
- vasoconstrictor
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