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Renin-Angiotensin System in Cardiovascular Biology, 2nd Edition
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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 4207

Special Issue Editors

Dr. Mária Szekeres

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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
Special Issues, Collections and Topics in MDPI journals
Dr. György L. Nádasy

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
Dr. László Dézsi

E-Mail Website
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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

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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Related Special Issue

Published Papers (3 papers)

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Research

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15 pages, 944 KB  
Article
Association Between the Renin–Angiotensin System and Ibrutinib-Related Cardiovascular Adverse Events: A Translational Cohort Study
by Jonaz Font, Amir Hodzic, Angélique Da-Silva, Baptiste Delapierre, Ghandi Damaj, Anne Neusy, Anne-Flore Plane, Damien Legallois, Paul Milliez, Charles Dolladille, Mégane Vernon, Sarah Burton, Nicolas Vigneron, Christophe Denoyelle and Joachim Alexandre
Biomedicines 2025, 13(9), 2184; https://doi.org/10.3390/biomedicines13092184 - 6 Sep 2025
Viewed by 812
Abstract
Background: Ibrutinib has been associated with an increased risk of cardiovascular adverse events (CVAEs), including atrial fibrillation (AF), hypertension (HTN), heart failure (HF), and ventricular arrhythmias (VAs). However, baseline predictors of CVAEs remain poorly characterized. In this study, we sought to identify baseline [...] Read more.
Background: Ibrutinib has been associated with an increased risk of cardiovascular adverse events (CVAEs), including atrial fibrillation (AF), hypertension (HTN), heart failure (HF), and ventricular arrhythmias (VAs). However, baseline predictors of CVAEs remain poorly characterized. In this study, we sought to identify baseline patient characteristics associated with the occurrence of ibrutinib-related CVAEs, with particular emphasis on parameters linked to the renin–angiotensin system. Methods: We conducted a prospective, single-center cohort study of consecutive patients treated with ibrutinib for B-cell malignancy, with systematic assessment of a predefined panel of potential predictors of CVAEs at baseline (NCT03678337). These predictors included demographic and clinical variables, 16 circulating biomarkers related to inflammation, fibrosis, and neurohormonal activation, as well as nine echocardiographic parameters. The primary objective was to evaluate the association between baseline patient characteristics and the occurrence of CVAEs from ibrutinib initiation through the end of follow-up. The CVAE endpoint was defined as a composite of atrial fibrillation, new or worsening hypertension, new or worsening heart failure, and ventricular arrhythmias. Statistical analyses were performed using the Wilcoxon–Mann–Whitney test or Fisher’s exact test, with a p-value < 0.05 considered statistically significant. Results: Among the 25 patients included, 7 experienced a total of 9 CVAEs over a median follow-up of 672 days. Elevated baseline plasma renin levels (>1336.10 pg/mL) were significantly associated with CVAEs occurrence (57% vs. 11%, p = 0.032). Higher baseline plasma aldosterone levels (>488.95 pg/mL) were also observed in patients who developed CVAEs, although this association did not reach statistical significance (p = 0.058). Conclusions: Baseline plasma renin level was univariably associated with CVAEs occurrence, while plasma aldosterone levels were higher among patients with CVAEs but did not reach statistical significance. These findings provide preliminary insights into the mechanisms underlying ibrutinib-related cardiovascular toxicity, suggesting a potential role for the renin–angiotensin–aldosterone system. Confirmation of this hypothesis, however, will require larger, dedicated studies. Full article
(This article belongs to the Special Issue Renin-Angiotensin System in Cardiovascular Biology, 2nd Edition)
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27 pages, 3323 KB  
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
Cited by 2 | Viewed by 918
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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Review

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19 pages, 1204 KB  
Review
Immunomodulatory Effects of RAAS Inhibitors: Beyond Hypertension and Heart Failure
by Raluca Ecaterina Haliga, Elena Cojocaru, Oana Sîrbu, Ilinca Hrițcu, Raluca Elena Alexa, Ioana Bianca Haliga, Victorița Șorodoc and Adorata Elena Coman
Biomedicines 2025, 13(7), 1779; https://doi.org/10.3390/biomedicines13071779 - 21 Jul 2025
Cited by 3 | Viewed by 1228
Abstract
The renin–angiotensin–aldosterone system (RAAS) plays a central role in cardiovascular and renal homeostasis and is increasingly recognized for its broad immunomodulatory effects. Pharmacological RAAS inhibition, primarily via angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), has demonstrated therapeutic value beyond its use [...] Read more.
The renin–angiotensin–aldosterone system (RAAS) plays a central role in cardiovascular and renal homeostasis and is increasingly recognized for its broad immunomodulatory effects. Pharmacological RAAS inhibition, primarily via angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs), has demonstrated therapeutic value beyond its use in hypertension and heart failure, extending to autoimmune, infectious, oncologic, and neurodegenerative conditions. ACEIs and ARBs modulate both innate and adaptive immune responses through Ang II-dependent and -independent mechanisms, influencing macrophage polarization, T-cell differentiation, cytokine expression, and antigen presentation. Notably, ACEIs exhibit Ang II-independent effects by enhancing antigen processing and regulating amyloid-β metabolism, offering potential neuroprotective benefits in Alzheimer’s disease. ARBs, particularly telmisartan and candesartan, provide additional anti-inflammatory effects via PPARγ activation. In cancer, RAAS inhibition affects tumor growth, angiogenesis, and immune surveillance, with ACEIs and ARBs showing distinct yet complementary impacts on tumor microenvironment modulation and chemotherapy cardioprotection. Moreover, ACEIs have shown promise in autoimmune myocarditis, colitis, and diabetic nephropathy by attenuating inflammatory cytokines. While clinical evidence supports the use of centrally acting ACEIs to treat early cognitive decline, further investigation is warranted to determine the long-term outcomes across disease contexts. These findings highlight the evolving role of RAAS inhibitors as immunomodulatory agents with promising implications across multiple systemic pathologies. Full article
(This article belongs to the Special Issue Renin-Angiotensin System in Cardiovascular Biology, 2nd Edition)
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