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From Kidney Disease to Hypertension: Molecular Basis and Pathophysiology
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From Kidney Disease to Hypertension: Molecular Basis and Pathophysiology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 January 2026 | Viewed by 3879

Special Issue Editor

Dr. Alexis A. Gonzalez

E-Mail Website
Guest Editor
Institute of Chemisry, Pontificia Universidad Católica de Valparaíso, Valparaíso 2950, Chile
Interests: renal system; renal injury; arterial hypertension; renal dysfunction; renin–angiotensin system
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The intricate relationship between kidney disease and hypertension underscores a significant area of research, as kidney dysfunction often leads to or exacerbates high blood pressure. The molecular mechanisms underlying this connection involve interactions within the renin-angiotensin-aldosterone system (RAAS), endothelial cell dysfunction, systemic inflammation, and other complex mechanisms. Recent studies have shed light on how these pathways contribute to the development and progression of both conditions, revealing potential new targets for therapeutic intervention.

This special issue aims to delve into the intricate mechanisms that underlie the complex relationship between kidney disease and hypertension. Whether it's deciphering novel cellular and molecular mechanisms, elucidating regulatory networks, or examining genes that contribute to the advancement of hypertension associated with renal pathologies, we invite researchers from diverse fields to share their groundbreaking insights and contributions to this special issue. We aim to offer novel insights into the pathophysiological processes involved in kidney-related hypertension, thereby illuminating potential avenues for the development of innovative treatment strategies. 

Dr. Alexis A. Gonzalez
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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-aldosterone system
  • endothelial cell dysfunction
  • systemic inflammation
  • hypertension
  • oxidative stress
  • vascular remodeling

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Related Special Issue

Published Papers (3 papers)

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Research

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14 pages, 1190 KB  
Article
Expression of the Renin-Angiotensin System in the Heart, Aorta, and Perivascular Adipose Tissue in an Animal Model of Type 1 Diabetes
by Beatriz Martín-Carro, Sara Fernández-Villabrille, Paula Calvó-García, Nerea González-García, Francisco Baena-Huerta, Angie Hospital-Sastre, Pedro Pujante, Francisco José López-Hernández, Manuel Naves-Díaz, Sara Panizo, Natalia Carrillo-López, Cristina Alonso-Montes and José Luis Fernández-Martín
Int. J. Mol. Sci. 2025, 26(19), 9538; https://doi.org/10.3390/ijms26199538 - 29 Sep 2025
Abstract
This study examined the expression of the renin-angiotensin system (RAS) and inflammatory markers in cardiovascular complications associated with long-term type 1 diabetes (T1D) using a rat model. After 24 weeks of streptozotocin-induced T1D, the animals exhibited metabolic alterations indicative of both cardiac and [...] Read more.
This study examined the expression of the renin-angiotensin system (RAS) and inflammatory markers in cardiovascular complications associated with long-term type 1 diabetes (T1D) using a rat model. After 24 weeks of streptozotocin-induced T1D, the animals exhibited metabolic alterations indicative of both cardiac and renal dysfunction. Tissue-specific dysregulation of RAS components and pro-inflammatory markers were observed in the heart, aorta, and perivascular adipose tissue (PVAT). In the heart, there was a significant upregulation of both classical (AT1R, 1.00 (0.22) vs. 1.70 (0.45) R.U.) and counter-regulatory RAS components (ACE2, 1.00 (0.43) vs. 1.96 (0.67) R.U.; p < 0.001) and MasR (1.00 (0.56) vs. 1.33 (0.29) R.U.; p = 0.004). The aorta displayed increased expression of classical RAS components alongside a significant reduction in ACE2 expression (1.00 (0.74) vs. 0.51 (0.48) R.U.; p < 0.032). Notably, PVAT showed a significant overexpression of classical RAS components (ACE 1.00 (0.22) vs. 4.08 (1.32) R.U.; p < 0.001, AT1R 1.00 (0.59) vs. 7.22 (4.14) R.U.; p < 0.001) and MasR (1.00 (0.70) vs. 4.52 (1.91) R.U.; p < 0.001), accompanied by increased expression of TNFα and ADAM17. These findings suggest that long-term T1D induces tissue-specific activation patterns of the RAS and inflammatory pathways within the cardiovascular system, which may contribute to the progression of diabetic cardiovascular complications. Therapeutic targeting of RAS components may represent a viable strategy for mitigating cardiovascular damage in T1D. Full article
(This article belongs to the Special Issue From Kidney Disease to Hypertension: Molecular Basis and Pathophysiology)
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17 pages, 2386 KB  
Article
(Pro)renin Receptor Blockade Prevents Increases in Systolic Blood Pressure, Sodium Retention, and αENaC Protein Expression in the Kidney of 2K1C Goldblatt Mice
by Pilar Cárdenas, Catalina Cid-Salinas, Allison C. León, Juan Castillo-Geraldo, Lilian Caroline Gonçalves de Oliveira, Rodrigo Yokota, Zoe Vallotton, Dulce Elena Casarini, Minolfa C. Prieto, Ramón A. Lorca and Alexis A. Gonzalez
Int. J. Mol. Sci. 2025, 26(9), 4177; https://doi.org/10.3390/ijms26094177 - 28 Apr 2025
Viewed by 825
Abstract
Physiological control of blood pressure (BP) and extracellular fluid volume is mediated by the action of the renin-angiotensin system (RAS). The presence of RAS components throughout the nephron has been widely discussed. The (pro)renin receptor (PRR) is a member of the RAS widely [...] Read more.
Physiological control of blood pressure (BP) and extracellular fluid volume is mediated by the action of the renin-angiotensin system (RAS). The presence of RAS components throughout the nephron has been widely discussed. The (pro)renin receptor (PRR) is a member of the RAS widely expressed in the body of humans and rodents. In the kidney, PRR is expressed in mesangial cells, renal vasculature, and tubules of the proximal and distal nephron. Binding of the PRR to renin and prorenin promotes angiotensin (Ang) I-mediated sodium (Na+) reabsorption via the epithelial sodium channel (ENaC). The Goldblatt 2-kidney 1-clip (2K1C) is a model of experimental renovascular hypertension that displays activation of systemic and intrarenal RAS. We use the 2K1C hypertension mouse model for 7 days to evaluate the role of the PRR on renal αENaC expression, Na+ reabsorption, and BP using pharmacological systemic blockade of the PRR with PRO20 peptide. Mice undergoing or not to 2K1C surgery (0.13 mm clip internal gap) were chronically infused with PRO20 and compared to sham (control) mice to assess changes in systolic BP (SBP) and diastolic BP (DBP), intrarenal angiotensin-converting enzyme (ACE) activity, Ang II, and renal αENaC expression and natriuretic responses after a saline challenge. Renal artery obstruction increased SBP and DBP, intrarenal ACE activity, Ang II levels, Na+ retention, and αENaC expression in both kidneys. PRO20 prevented the increases in SBP, DBP, attenuated Na+ retention, and blunted intrarenal Ang II and αENaC levels in non-clipped kidneys of 2K1C mice. Chronic infusion of the PRR for 7 days prevents hypertensive responses in part due to impaired αENaC upregulation and intrarenal Ang II formation in the early phase of the development of renovascular hypertension in 2K1C Goldblatt mice. Full article
(This article belongs to the Special Issue From Kidney Disease to Hypertension: Molecular Basis and Pathophysiology)
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Review

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20 pages, 950 KB  
Review
Kidney Programming and Hypertension: Linking Prenatal Development to Adulthood
by You-Lin Tain and Chien-Ning Hsu
Int. J. Mol. Sci. 2024, 25(24), 13610; https://doi.org/10.3390/ijms252413610 - 19 Dec 2024
Cited by 2 | Viewed by 2132
Abstract
The complex relationship between kidney disease and hypertension represents a critical area of research, yet less attention has been devoted to exploring how this connection develops early in life. Various environmental factors during pregnancy and lactation can significantly impact kidney development, potentially leading [...] Read more.
The complex relationship between kidney disease and hypertension represents a critical area of research, yet less attention has been devoted to exploring how this connection develops early in life. Various environmental factors during pregnancy and lactation can significantly impact kidney development, potentially leading to kidney programming that results in alterations in both structure and function. This early programming can contribute to adverse long-term kidney outcomes, such as hypertension. In the context of kidney programming, the molecular pathways involved in hypertension are intricate and include epigenetic modifications, oxidative stress, impaired nitric oxide pathway, inappropriate renin–angiotensin system (RAS) activation, disrupted nutrient sensing, gut microbiota dysbiosis, and altered sodium transport. This review examines each of these mechanisms and highlights reprogramming interventions proposed in preclinical studies to prevent hypertension related to kidney programming. Given that reprogramming strategies differ considerably from conventional treatments for hypertension in kidney disease, it is essential to shift focus toward understanding the processes of kidney programming and its role in the development of programmed hypertension. Full article
(This article belongs to the Special Issue From Kidney Disease to Hypertension: Molecular Basis and Pathophysiology)
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