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Genomic and Molecular Landscapes of Cardiac Remodeling and Heart Failure
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Genomic and Molecular Landscapes of Cardiac Remodeling and Heart Failure

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Genetic Diagnosis".

Deadline for manuscript submissions: 20 April 2026 | Viewed by 737

Special Issue Editor

Dr. Dorota Ciołczyk-Wierzbicka

E-Mail Website
Guest Editor
Center for Medical Genomics—OMICRON, Jagiellonian University Medical College, ul. Kopernika 7c, 31-034 Kraków, Poland
Interests: gene expression; cell line; Molecular; cardiomyopathy; cancer therapy

Special Issue Information

Dear Colleagues,

Heart failure remains one of the leading causes of morbidity and mortality worldwide, with myocardial remodeling and fibrosis being central hallmarks of disease progression. Advances in genomics, transcriptomics, epigenetics, and non-coding RNAs are providing new insights into the molecular pathways underlying cardiac dysfunction, while translational approaches offer novel opportunities for early diagnosis and therapy.

This Special Issue of Genes aims to provide a broad and interdisciplinary platform for studies addressing the genetic, molecular, and cellular mechanisms of heart failure, highlighting discoveries that bridge basic research with clinical application. We welcome the submission of original research, reviews, and methodological papers focused on, but not limited to, the following:

  • Genomic and transcriptomic profiling in heart failure and cardiomyopathies;
  • Epigenetic regulation and chromatin remodeling in cardiac disease;
  • Non-coding RNAs (miRNA, lncRNA, circRNA) in cardiac pathophysiology;
  • Molecular and cellular mechanisms of myocardial fibrosis and regeneration;
  • Multiomics, bioinformatics, and AI-driven approaches to cardiac genomics;
  • Translational perspectives and therapeutic applications of genomic discoveries.

The goal of this Special Issue is to explore the genomic and molecular signatures shaping cardiac remodeling, identify novel biomarkers and therapeutic targets, and contribute to the development of precision cardiology.

Dr. Dorota Ciołczyk-Wierzbicka
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 250 words) can be sent to the Editorial Office for assessment.

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. Genes 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

  • heart failure
  • genomics
  • transcriptomics
  • epigenetics/chromatin remodeling
  • non-coding RNAs
  • myocardial fibrosis
  • cardiac regeneration
  • multi-omics & AI-driven bioinformatics
  • precision cardiology
  • translational therapeutics
 

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Published Papers (2 papers)

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Research

12 pages, 453 KB  
Article
Association Analyses Between the NPPB:rs198389 Gene Polymorphism, NT-proBNP Serum Concentrations and Phenotypic Features in Patients with Heart Failure
by Anna Gorący-Rosik, Jakub Rosik, Klaudyna Lewandowska, Iwona Gorący and Andrzej Ciechanowicz
Genes 2026, 17(4), 454; https://doi.org/10.3390/genes17040454 - 14 Apr 2026
Abstract
Background: Heart failure (HF) is a complex disease and one of the major causes of morbidity and mortality in the world. Increased B-type natriuretic peptide (BNP) levels have been associated with HF. The NPPB:rs198389 (c.-381T > C) promoter polymorphism has been found [...] Read more.
Background: Heart failure (HF) is a complex disease and one of the major causes of morbidity and mortality in the world. Increased B-type natriuretic peptide (BNP) levels have been associated with HF. The NPPB:rs198389 (c.-381T > C) promoter polymorphism has been found to modulate BNP levels. Aim: To investigate possible associations among the NPPB:rs198389 polymorphism, N-terminal pro-BNP (NT-proBNP) concentrations, and phenotypic features in Polish patients with HF. Methods: The study group comprised 250 patients with HF. Genomic DNA was extracted from blood, and genotyping was performed using PCR-RFLP. Results: There were no significant differences in the distributions of NPPB genotypes or alleles between HF females and HF males. Except for body height, there were no significant differences in phenotypic features among HF patients regarding NPPB:rs198389 genotypes. There were also no significant differences in the distributions of either NPPB:rs198389 genotypes or alleles across NT-proBNP concentration terciles. However, age, left-ventricular-mass index, C-reactive-protein levels, serum-creatinine concentrations, and the incidence of myocardial infarction, left ventricular hypertrophy, or reduced ejection fraction (EF) were significantly lower in patients from the lower tercile (LT) than in patients from the middle and/or upper terciles. EF and the frequency of preserved EF in LT patients were significantly higher than those from other terciles. Conclusions: Our results did not confirm associations between NPPB:rs198389 and NT-proBNP serum concentrations or clinical phenotypes in Polish patients with HF. Full article
(This article belongs to the Special Issue Genomic and Molecular Landscapes of Cardiac Remodeling and Heart Failure)
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17 pages, 580 KB  
Article
Early Detection of Pacing-Induced Cardiomyopathy Using MicroRNA-208b-3p and MicroRNA-9: A Prospective Cohort Analysis
by Onoufrios Malikides, Aleksi Sallo, Andria Papazachariou, Ioannis Kopidakis, Angeliki Alifragki, Joanna Kontaraki, Konstantinos Fragkiadakis, Gregory Chlouverakis, Eleftherios Kallergis, Emmanuel Simantirakis and Maria Marketou
Genes 2026, 17(1), 103; https://doi.org/10.3390/genes17010103 - 19 Jan 2026
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Abstract
Background/Objectives: Pacing-induced cardiomyopathy (PiCM) is a recognized complication of chronic right ventricular pacing (RVP), characterized by left ventricular (LV) dysfunction, adverse remodeling, and progression to heart failure. MicroRNAs (miRs) regulate gene expression and play an important role in ventricular remodeling. This study aimed [...] Read more.
Background/Objectives: Pacing-induced cardiomyopathy (PiCM) is a recognized complication of chronic right ventricular pacing (RVP), characterized by left ventricular (LV) dysfunction, adverse remodeling, and progression to heart failure. MicroRNAs (miRs) regulate gene expression and play an important role in ventricular remodeling. This study aimed to observe whether dynamic changes in miRs according to a novel peripheral blood mononuclear cell (PBMC)-based approach could serve as early predictive biomarkers of PiCM. Methods: A prospective, single-center cohort study was conducted in adult patients undergoing pacemaker implantation. Clinical characteristics, echocardiographic parameters and expression levels of miR-208b-3p and miR-9 were assessed immediately and 3 months post-pacemaker implantation. PiCM was defined as a ≥10% reduction in LVEF at one year, with no alternative cause. Statistical analyses included correlation testing, ROC curve analysis, and multivariate regression to identify factors associated with PiCM. Results: Among 126 patients, 11.1% developed PiCM. Compared with the non-PiCM group, those who developed PiCM exhibited more pronounced 3-month changes in miR-208b-3p (median Δ3log miR: +1.3 vs. −0.4, p = 0.013) and miR-9 (median Δ3log miR: −1.7 vs. +0.21, p = 0.011). In multivariate analyses, Δ3LV-GLS, Δ3logmiR-208b-3p, and Δ3logmiR-9 were associated with a higher likelihood of PiCM. Among PiCM patients, Δ3logmiR-208b-3p correlated inversely with Δ3LV-GLS (r = −0.73, p = 0.016), while Δ3logmiR-9 correlated positively (r = 0.88, p < 0.001). ROC analyses demonstrated good predictive ability for Δ3LV-GLS (AUC = 0.924), Δ3log miR-208b-3p (AUC = 0.783), and Δ3log miR-9 (AUC = 0.835), with no significant differences between curves. Conclusions: Early LV-GLS deterioration and dynamic changes in expression of miR-208b-3p and miR-9 in PBMCs precede overt LV systolic dysfunction. These miRs may serve as early predictive biomarkers for PiCM. Full article
(This article belongs to the Special Issue Genomic and Molecular Landscapes of Cardiac Remodeling and Heart Failure)
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