Renin-Angiotensin System in Cardiovascular Biology, 2nd Edition

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1021

Special Issue Editors


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Guest Editor
Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University, 1088 Budapest, Hungary
Interests: renin-angiotensin system (RAS); vascular; vascular remodeling; hypertension; atherosclerosis; endocannabinoid system
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E-Mail Website
Guest Editor
Department of Physiology, Faculty of Medicine, Semmelweis University, 1094 Budapest, Hungary
Interests: cardiovascular physiology; angiotensin II; renin-angiotensin system (RAS); vascular; hypertension; coronary vessels; cerebral vessels
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Translational Medicine Institute, Semmelweis University, Nagyvarad ter 4, 1089 Budapest, Hungary
Interests: cardiovascular physiology & pharmacology; renin-angiotensin system (RAS); local blood flow control; hypersensititvity reaction (HSR); nanomedicines; complement; CARPA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Based on our successful Special Issue on the same topic entitled "Renin-Angiotensin System in Cardiovascular Biology" (Biomedicines | Special Issue : Renin-Angiotensin System in Cardiovascular Biology (mdpi.com)), we have launched a 2nd edition of the Special Issue.

The aim of this Special Issue is to present the latest updates on the role of the renin-angiotensin system (RAS) in cardiovascular biology, from cellular mechanisms to organ functions and novel therapeutic mechanisms. The RAS has an important role in the regulation of blood pressure and salt water homeostasis. Angiotensin II (AngII) is the main regulator, which operates by stimulating AT1 receptors, a member of the G protein-coupled receptor family, and activating mainly calcium signaling mechanisms inducing, e.g., smooth muscle contraction, vasoconstriction and blood pressure elevation. Long-term overactivation of the RAS may result in inflammatory mechanisms, vascular hypertrophy and remodeling, water retention, hypertension and atherosclerosis. Therapies based on angiotensin-converting enzyme (ACE) inhibitors (ACEIs) and blockers of AT1 angiotensin receptors have been effectively used in the therapy of hypertension for decades. Other RAS pathways have more recently become the focus of research, including ACE2 and AT2 receptor signaling, as well as the conversion of AngII to Ang 1–7, which may provide links between the deleterious and beneficial actions of RAS. Alternative activation of these pathways may also propose novel additional molecular mechanisms and beneficial therapeutic potential in cardiovascular pathology.

This Special Issue therefore invites original research papers and review articles providing the latest insights into the complexity of the cell signaling and biological mechanisms of the RAS components to propose novel mechanisms in cardiovascular physiology and pathophysiology. By targeting this system, works may provide novel therapeutic potential in cardiovascular and related diseases such as hypertension, heart failure, atherosclerosis and diabetes mellitus.

Dr. Mária Szekeres
Dr. György L. Nádasy
Dr. László Dézsi
Guest Editors

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Keywords

  • renin–angiotensin system (RAS)
  • signaling mechanisms of angiotensin receptors
  • GPCR
  • AT1R
  • AT2R
  • ACE
  • ACE2
  • ACEI
  • angiotensin II
  • signal transduction
  • cardiovascular system
  • hypertension
  • atherosclerosis
  • heart failure
  • cardiovascular remodeling
  • osmoregulation
  • inflammation

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Published Papers (1 paper)

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Research

27 pages, 3323 KiB  
Article
Inhibition of the Renin–Angiotensin System Improves Hemodynamic Function of the Diabetic Rat Heart by Restoring Intracellular Calcium Regulation
by Krisztina Anna Paulik, Tamás Ivanics, Gábor A. Dunay, Ágnes Fülöp, Margit Kerék, Klára Takács, Zoltán Benyó and Zsuzsanna Miklós
Biomedicines 2025, 13(3), 757; https://doi.org/10.3390/biomedicines13030757 - 20 Mar 2025
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Abstract
Background/Objectives: Disrupted intracellular calcium (Ca2+i) regulation and renin–angiotensin system (RAS) activation are pathogenetic factors in diabetic cardiomyopathy, a major complication of type 1 (T1D) and type 2 (T2D) diabetes. This study explored their potential link in diabetic rat hearts. Methods: [...] Read more.
Background/Objectives: Disrupted intracellular calcium (Ca2+i) regulation and renin–angiotensin system (RAS) activation are pathogenetic factors in diabetic cardiomyopathy, a major complication of type 1 (T1D) and type 2 (T2D) diabetes. This study explored their potential link in diabetic rat hearts. Methods: Experiments were conducted on T1D and T2D Sprague-Dawley rats induced by streptozotocin and fructose-rich diet, respectively. In T1D, rats were treated with Enalapril (Ena) or Losartan (Los) for six weeks, whereas T2D animals received high-dose (HD) or low-dose (LD) Ena for 8 weeks. Heart function was assessed via echocardiography, Ca2+i transients by Indo-1 fluorometry in Langendorff-perfused hearts, and key Ca2+i cycling proteins by Western blot. Data: mean ± SD. Results: Diabetic hearts exhibited reduced contractile performance that was improved by RAS inhibition both in vivo (ejection fraction (%): T1D model: Control: 79 ± 7, T1D: 54 ± 11, T1D + Ena: 65 ± 10, T1D + Los: 69 ± 10, n = 18, 18, 15, 10; T2D model: Control: 73 ± 8, T2D: 52 ± 6, T2D + LDEna: 62 ± 8, T2D + HDEna: 76 ± 8, n = 9, 8, 6, 7) and ex vivo (+dPressure/dtmax (mmHg/s): T1D model: Control: 2532 ± 341, T1D: 2192 ± 208, T1D + Ena: 2523 ± 485, T1D + Los: 2643 ± 455; T2D model: Control: 2514 ± 197, T2D: 1930 ± 291, T2D + LDEna: 2311 ± 289, T2D + HDEna: 2614 ± 268). Analysis of Ca2+i transients showed impaired Ca2+i release and removal dynamics and increased diastolic Ca2+i levels in both models that were restored by Ena and Los treatments. We observed a decrease in sarcoendoplasmic reticulum Ca2+-ATPase2a (SERCA2a) expression, accompanied by a compensatory increase in 16Ser-phosphorylated phospholamban (P-PLB) in T2D that was prevented by both LD and HD Ena (expression level (% of Control): SERCA2a: T2D: 36 ± 32, T2D + LDEna: 112 ± 32, T2D + HDEna: 106 ± 30; P-PLB: T2D: 557 ± 156, T2D + LDEna: 129 ± 38, T2D + HDEna: 108 ± 42; n = 4, 4, 4). Conclusions: The study highlights the critical role of RAS activation, most likely occurring at the tissue level, in disrupting Ca2+i homeostasis in diabetic cardiomyopathy. RAS inhibition with Ena or Los mitigates these disturbances independent of blood pressure effects, underlining their importance in managing diabetic heart failure. Full article
(This article belongs to the Special Issue Renin-Angiotensin System in Cardiovascular Biology, 2nd Edition)
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