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Molecular Mechanisms and Pharmacological Underlying Cardiorenal Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (31 October 2025) | Viewed by 531

Special Issue Editor


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Guest Editor
Unit of Nephrology and Dialysis, Hypertension Excellence Centre, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), University of Palermo, 90133 Palermo, Italy
Interests: nephrocardiology; chronic renal failure; hypertension
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Special Issue Information

Dear Colleagues,

A growing body of medical literature underscores the intricate relationship between the heart and kidneys, both in terms of their physiological functions and underlying molecular mechanisms. It is becoming increasingly clear that cardiology and nephrology are closely interconnected, and numerous studies emphasize the need for a collaborative and interdisciplinary approach to understanding these interactions. Moreover, the rising prevalence of diabetes has exacerbated this relationship within the broader context of cardio-renal-metabolic syndrome.

Pharmacological and molecular research has yielded innovative therapeutic agents that show promise in addressing the complex interplay between these organs. In this Special Issue, we aim to deepen our understanding of the pharmacological and molecular mechanisms underlying cardio-renal disease, with a focus on the development of novel drug targets and therapeutic strategies.

We invite your valuable contributions to this exciting area of research, as we strive to expand our knowledge and enhance therapeutic approaches to treating cardio-renal dysfunction at the molecular level.

Dr. Caterina Carollo
Guest Editor

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Keywords

  • hypertension
  • cardio-renal syndromes
  • heart failure
  • chronic kidney disease
  • hemodialysis
  • periotenal dialysis

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Published Papers (1 paper)

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Research

25 pages, 6158 KB  
Article
Hydrogen Sulfide and Nitric Oxide Improve Renal Function and α-Adrenergic Responsiveness in Rats with Left Ventricular Hypertrophy
by Tabinda Fatima, Latifah Al Shammari, Mohamed Ibrahim Lazhari, Waad Alrohily, Tan Yong Chia, Nimer Alsabeelah, Eid Fahad Alanazi, Khalid Abdulrahman Almutairi, Sultan Mujahid Alhabradi, Naif Saleh Alharbi and Ashfaq Ahmad
Curr. Issues Mol. Biol. 2025, 47(10), 848; https://doi.org/10.3390/cimb47100848 - 15 Oct 2025
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Abstract
In left ventricular hypertrophy (LVH), the combined external administration of hydrogen sulfide (H2S) and nitric oxide (NO) has been shown to reverse LVH by activating the endothelial nitric oxide synthase pathway (eNOS/NO), independent of the cystathionine γ-lyase (CSE/H2S) pathway. [...] Read more.
In left ventricular hypertrophy (LVH), the combined external administration of hydrogen sulfide (H2S) and nitric oxide (NO) has been shown to reverse LVH by activating the endothelial nitric oxide synthase pathway (eNOS/NO), independent of the cystathionine γ-lyase (CSE/H2S) pathway. Individually, both H2S and NO have also been reported to significantly improve RCBP, restore renal excretory performance, and enhance α-adrenergic receptor responsiveness in rats. The induction of LVH was performed over a period of two weeks using drinking water with caffeine and isoprenaline. Five weeks later, the rats were fed with L-arginine (1.25 g/L) as a nitrogen oxide donor. Vascular reactions to methoxamine, phenylephrine, and noradrenaline were assessed in presences and absence of 5-methylurapidil (5-MeU), BMY7378, and chloroethylclonidine (CeC) and α1-adrenoceptor antagonists. In both the Control WKY and LVH-WKY groups, combined H2S+NO therapy significantly (p < 0.05) upregulated the renal mRNA of CSE and eNOS when compared with untreated LVH rats. The treatment also markedly increased RCBP in LVH-H2S+NO rats relative to LVH controls. Furthermore, H2S+NO administration enhanced the activity of α1A, α1B, and α1D adrenergic receptors in mediating renal vasoconstriction. Even under receptor blockade with high doses (HDs) of 5-MeU, CeC, and BMY 7378, renal vasoconstriction responses to adrenergic agonists like NA, PE, and ME in the LVH-H2S+NO group remained comparable to those observed in the counterpart Control-H2S+NO group. The findings of current study suggest that simultaneous exogenous administration of H2S and NO donors improve renal cortical blood flow, support renal function, and augment α1A, α1B, and α1D adrenergic receptor responsiveness to adrenergic agonists like NA, PE, and ME in LVH rats. This effect appears to rely primarily on the eNOS/NO pathway, with partial contribution from the CSE/H2S pathway. Full article
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