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Molecular Mechanisms and Pharmacological Underlying Cardiorenal Diseases

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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: 31 May 2026 | Viewed by 2169

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Dr. Caterina Carollo

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Unit of Nephrology and Dialysis, Department of Health Promotion, Mother and Child Care, Internal Medicine and Medical Specialties (PROMISE), Hypertension Excellence Centre, University of Palermo, 90133 Palermo, Italy
Interests: nephrology; hypertension; dialysis; nephrocardiology; cardiorenal syndromes; diabetic nephropathy
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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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18 pages, 759 KB

Open AccessArticle

Differential TET1/2/3 Protein Expression in Circulating Leukocytes of Statin-Treated Patients with HFrEF

by Anna Wołowiec, Łukasz Wołowiec, Albert Jaśniak, Grzegorz Grześk, Jacek Budzyński, Joanna Osiak-Gwiazdowska, Paulina Jakubowska, Paweł Gordon and Mariusz Kozakiewicz

Curr. Issues Mol. Biol. 2026, 48(5), 467; https://doi.org/10.3390/cimb48050467 - 30 Apr 2026

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Abstract

Epigenetic mechanisms, including DNA methylation and hydroxymethylation, contribute to inflammation, cardiac remodelling and progression of heart failure. Ten–Eleven Translocation (TET) dioxygenases are key regulators of these processes, but the impact of statins on TET proteins in human heart failure is not well characterised. We investigated how statin therapy relates to TET1, TET2 and TET3 expression in circulating immune cells in heart failure with reduced ejection fraction (HFrEF). In this cross-sectional study, 106 patients with HFrEF were enrolled; 84 were receiving statins and 22 were not. Intracellular TET1/2/3 protein levels were measured by multiparameter flow cytometry in granulocytes, monocytes and lymphocytes, and clinical and laboratory characteristics were compared between groups. Statin-treated patients had lower NT-proBNP concentrations and lower neutrophil, lymphocyte and monocyte counts, and more often received guideline-directed medical therapy. Statin therapy was associated with a distinct TET expression profile, characterised by higher TET1 and TET3 indices in monocytes and lymphocytes and lower TET2 indices in granulocytes and monocytes. This pattern is compatible with a distinct immune-cell TET expression profile aligned with the anti-inflammatory and reparative profile attributed to statins, and the course of disease. These associations do not establish causality and require prospective validation. TET proteins may form part of an epigenetic signature associated with statin treatment in heart failure and warrant further study as potential biomarkers in larger, prospective cohorts. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Underlying Cardiorenal Diseases)

16 pages, 4524 KB

Open AccessArticle

MicroRNA-451 Modulates Autophagy-Related Signaling with Relevance to Renal Fibrosis in an Accelerated Mouse Model of Diabetic Kidney Disease

by Chidera Obiwuma, Baiyee-Ndang Agbor-Baiyee, Sadaf Ghaderzadeh, Neal Mohit, Kanwal K. Gambhir, Bradley Bobga and Maurice B. Fluitt

Curr. Issues Mol. Biol. 2026, 48(2), 223; https://doi.org/10.3390/cimb48020223 - 19 Feb 2026

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Abstract

Background: Diabetic nephropathy is characterized by metabolic dysregulation, renal fibrosis, and impaired autophagy. MicroRNA-451 (miR-451) has been implicated in metabolic and stress-response pathways, but its role in diabetic kidney disease remains unclear. This study examined the effects of systemic miR-451 overexpression on renal injury and autophagy in BTBR ob/ob mice. Methods: Wild-type (WT) and BTBR ob/ob (OB) mice were treated with miR-451 mimics. Body weight, blood glucose, and urine albumin were assessed for three consecutive weeks. Renal miR-451 expression was measured by qRT-PCR, while protein levels of YWHAZ, mTOR, and autophagy markers were analyzed by Western blotting. Renal fibrosis was evaluated using Masson’s trichrome staining. Results: OB mice exhibited increased body weight, hyperglycemia, and albuminuria compared with WT controls. miR-451 treatment resulted in robust renal overexpression of miR-451 in OB treated mice (8.4-fold, p = 0.039) but did not normalize metabolic parameters. miR-451 overexpression significantly reduced renal expression of YWHAZ and mTOR. Histological analysis revealed increased glomerular fibrosis in OB mice, which was significantly attenuated following miR-451 treatment in WT-treated and OB-treated mice. In addition, miR-451 treatment increased expression of autophagy-related proteins ATG101 and Beclin-1 and reduced the LC3-II/I ratio, indicating altered autophagic signaling. Conclusions: miR-451 overexpression attenuates renal fibrosis and modulates autophagy-associated pathways in diabetic kidney disease, independent of metabolic control, highlighting miR-451 as a potential therapeutic target for diabetic kidney disease. Full article

(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Underlying Cardiorenal Diseases)

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25 pages, 6158 KB

Open AccessArticle

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

Cited by 1 | Viewed by 1005

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. 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 α_1A, α_1B, and α_1D 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 α_1A, α_1B, and α_1D 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

(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Underlying Cardiorenal Diseases)

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