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The Angiotensin in Human Health and Diseases
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The Angiotensin in Human Health and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 12230

Special Issue Editor

Prof. Dr. Helmy M. Siragy

E-Mail Website
Guest Editor
Division of Endocrinology and Metabolism, Department of Medicine University of Virginia Health System, Charlottesville, VA 22908, USA
Interests: renin–angiotensin–aldosterone system; endocrine hypertension; adrenal gland; diabetic kidney disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The renin angiotensin aldosterone system (RAAS) plays an important role in the control of body fluid and electrolyte homeostasis, as well as in blood pressure regulation. Angiotensin II is the most important effector hormone in this system and functions primarily through the stimulation of its subtype receptors, in particular the AT1 receptor. The knowledge about the involvement of other angiotensin receptors in physiological and pathological processes is still evolving. RAAS contributes to the regulation of cardiovascular, renal and metabolic functions. Additionally, RAAS regulates cellular growth and matrix formation. The imbalance of RAAS function has been linked to multiple cardiovascular, renal and metabolic diseases. This Special Issue will focus on the evolving knowledge involving RAAS activities in human health and disease.

Prof. Dr. Helmy M. Siragy
Guest Editor

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Keywords

  • renin–angiotensin–aldosterone system
  • angiotensin subtype receptors
  • cardiovascular disease
  • kidney diseases
  • stroke
  • metabolic abnormalities
  • obesity and adipose tissue
  • oxidative stress and inflammation
  • blood pressure and salt sensitivity

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Published Papers (4 papers)

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Research

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16 pages, 4245 KiB  
Article
Aldosterone-Induced Transformation of Vascular Smooth Muscle Cells into Macrophage-like Cells Participates in Inflammatory Vascular Lesions
by Boya Zhang, Ziqian Liu, Yi Chang, Ruyan Lv, Haixia Guo, Panpan Qiang, Tatsuo Shimosawa, Qingyou Xu and Fan Yang
Int. J. Mol. Sci. 2025, 26(7), 3345; https://doi.org/10.3390/ijms26073345 - 3 Apr 2025
Viewed by 439
Abstract
Vascular smooth muscle cells (VSMCs) are the most abundant cell type in blood vessels, participating in cardiovascular diseases in various ways, among which their transformation into macrophage-like cells has become a research hotspot. In this study, rats were infused with aldosterone for 12 [...] Read more.
Vascular smooth muscle cells (VSMCs) are the most abundant cell type in blood vessels, participating in cardiovascular diseases in various ways, among which their transformation into macrophage-like cells has become a research hotspot. In this study, rats were infused with aldosterone for 12 weeks, and VSMCs stimulated with aldosterone in vitro were used to observe aortic injury and the role of VSMC transformation. Vascular changes were detected via small animal ultrasound and H&E staining. Moreover, immunohistochemistry, immunofluorescence, Western blot, and flow cytometry were used to verify that the transformation of VSMCs into macrophage-like cells is regulated by mineralocorticoid receptor (MR) activation and macrophage colony-stimulating factor (M-CSF) and its receptor. Rat vasculature and in vitro cellular experiments revealed that VSMCs transformed into macrophage-like cells and secreted inflammatory factors such as interleukin-1β (IL-1β) and monocyte chemoattractant protein-1 (MCP-1), thereby exacerbating inflammatory vascular lesions, which was inhibited by the MR antagonist esaxerenone. These results reveal that increased levels of aldosterone activate MR, leading to the secretion of M-CSF by VSMCs. This further promotes the transformation of VSMCs into macrophage-like cells, which participate in inflammatory vascular lesions. Therefore, inhibiting the formation of macrophage-like cells can effectively reduce inflammatory vascular lesions. Full article
(This article belongs to the Special Issue The Angiotensin in Human Health and Diseases)
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Review

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16 pages, 577 KiB  
Review
Augmented Intrarenal and Urinary Angiotensinogen in Diabetic Nephropathy: The Role of Isoflavones
by Masumi Kamiyama, Kotoe Iijima, Rema Okuzawa, Ruka Kawata, Airi Kimura, Yuki Shinohara, Ayana Shimada, Mika Yamanaka, Ayuka Youda and Tamami Iwamoto
Int. J. Mol. Sci. 2025, 26(4), 1443; https://doi.org/10.3390/ijms26041443 - 8 Feb 2025
Viewed by 850
Abstract
The circulating renin–angiotensin system (RAS) is an endocrine system with key functions in maintaining blood pressure, fluid volume, and electrolytes. The RAS in the kidney (intrarenal RAS) plays a critical role in the onset and progression of kidney diseases. However, the mechanism underlying [...] Read more.
The circulating renin–angiotensin system (RAS) is an endocrine system with key functions in maintaining blood pressure, fluid volume, and electrolytes. The RAS in the kidney (intrarenal RAS) plays a critical role in the onset and progression of kidney diseases. However, the mechanism underlying the onset and progression of diabetic nephropathy in relation to the expression and secretion of angiotensinogen (AGT) in the kidneys remains unclear. In this review, we present an overview of the intrarenal RAS and its role in diabetic nephropathy, as well as reviewing the evidence for the use of urinary AGT as a biomarker of this system in diabetic nephropathy. We also describe the roles of isoflavones in the context of diabetic nephropathy. The considered studies show that the intrarenal RAS—especially AGT—plays a diversified role in diabetic nephropathy; for instance, the increase in AGT due to oxidative stress is suppressed by polyphenols with antioxidant capacity, which is thought to affect the progression of diabetic nephropathy. Therefore, clarification of how polyphenols affect the onset and progression of diabetic nephropathy may provide insights into new treatments for this illness. Full article
(This article belongs to the Special Issue The Angiotensin in Human Health and Diseases)
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23 pages, 1234 KiB  
Review
The Renin–Angiotensin System in Liver Disease
by Mary S. McGrath and Brian J. Wentworth
Int. J. Mol. Sci. 2024, 25(11), 5807; https://doi.org/10.3390/ijms25115807 - 27 May 2024
Cited by 7 | Viewed by 3884
Abstract
The renin–angiotensin system (RAS) is a complex homeostatic entity with multiorgan systemic and local effects. Traditionally, RAS works in conjunction with the kidney to control effective arterial circulation, systemic vascular resistance, and electrolyte balance. However, chronic hepatic injury and resulting splanchnic dilation may [...] Read more.
The renin–angiotensin system (RAS) is a complex homeostatic entity with multiorgan systemic and local effects. Traditionally, RAS works in conjunction with the kidney to control effective arterial circulation, systemic vascular resistance, and electrolyte balance. However, chronic hepatic injury and resulting splanchnic dilation may disrupt this delicate balance. The role of RAS in liver disease, however, is even more extensive, modulating hepatic fibrosis and portal hypertension. Recognition of an alternative RAS pathway in the past few decades has changed our understanding of RAS in liver disease, and the concept of opposing vs. “rebalanced” forces is an ongoing focus of research. Whether RAS inhibition is beneficial in patients with chronic liver disease appears to be context-dependent, but further study is needed to optimize clinical management and reduce organ-specific morbidity and mortality. This review presents the current understanding of RAS in liver disease, acknowledges areas of uncertainty, and describes potential areas of future investigation. Full article
(This article belongs to the Special Issue The Angiotensin in Human Health and Diseases)
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19 pages, 1235 KiB  
Review
The Renin–Angiotensin System and Cardiovascular–Kidney–Metabolic Syndrome: Focus on Early-Life Programming
by You-Lin Tain and Chien-Ning Hsu
Int. J. Mol. Sci. 2024, 25(6), 3298; https://doi.org/10.3390/ijms25063298 - 14 Mar 2024
Cited by 16 | Viewed by 5965
Abstract
The identification of pathological links among metabolic disorders, kidney ailments, and cardiovascular conditions has given rise to the concept of cardiovascular–kidney–metabolic (CKM) syndrome. Emerging prenatal risk factors seem to increase the likelihood of CKM syndrome across an individual’s lifespan. The renin–angiotensin system (RAS) [...] Read more.
The identification of pathological links among metabolic disorders, kidney ailments, and cardiovascular conditions has given rise to the concept of cardiovascular–kidney–metabolic (CKM) syndrome. Emerging prenatal risk factors seem to increase the likelihood of CKM syndrome across an individual’s lifespan. The renin–angiotensin system (RAS) plays a crucial role in maternal–fetal health and maintaining homeostasis in cardiovascular, metabolic, and kidney functions. This review consolidates current preclinical evidence detailing how dysregulation of the RAS during pregnancy and lactation leads to CKM characteristics in offspring, elucidating the underlying mechanisms. The multi-organ effects of RAS, influencing fetal programming and triggering CKM traits in offspring, suggest it as a promising reprogramming strategy. Additionally, we present an overview of interventions targeting the RAS to prevent CKM traits. This comprehensive review of the potential role of the RAS in the early-life programming of CKM syndrome aims to expedite the clinical translation process, ultimately enhancing outcomes in cardiovascular–kidney–metabolic health. Full article
(This article belongs to the Special Issue The Angiotensin in Human Health and Diseases)
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