ijms-logo

Journal Browser

Journal Browser

Advances in Cardiovascular Remodeling

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: 29 August 2024 | Viewed by 1722

Special Issue Editor


E-Mail Website
Guest Editor
Faculty of Health Sciences, University Rey Juan Carlos, 28922 Alcorcón, Spain Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), ISCIII, 28029 Madrid, Spain
Interests: marfan syndrome; cardiovascular remodeling; hypertension; aortic disease; heart hypertrophy; diabetes; endoplasmic reticulum stress; mitochondrial stress; cardiotoxicity
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pathological cardiovascular remodeling is associated with fibrosis, inflammation and cellular dysfunction. Myocardial remodeling (MR) is a deleterious process characterized by gradual cardiac enlargement and cardiac dysfunction produced by the underlying disease process. It is characterized by molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart whereas vascular remodeling is the process of altering structure and arrangement in blood vessels through cell growth, cell death, cell migration, and production or degradation of the ECM. Myocardial fibrosis and vascular disease play an important role in the progression to heart failure and are a primary cause of myocardial infarction, stroke and ischemia. Both are the leading cause of morbidity and mortality in the Western world and a major public health problem in industrialized countries. Moreover, cardiovascular remodeling is accelerated in hypertensive disease, atherosclerosis, diabetes mellitus, chronic kidney disease, inflammatory disease, genetic abnormalities and lifestyle aspects (smoking). In recent years, a large number of preclinical studies have demonstrated that blunting load-induced hypertrophic growth of the left ventricle and reducing vascular hypertrophic remodeling and wall stiffness is possible. These studies have uncovered a potential new target of anti-remodeling therapy, which if true, may be key to impeding the progression of cardiovascular diseases.

Dr. María Galán
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

  • extracellular matrix
  • hypertension
  • diabetes
  • atherosclerosis
  • vascular dysfunction
  • inflammation
  • heart hypertrophy
  • heart failure
  • biomarkers
  • therapeutic targets

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

10 pages, 1795 KiB  
Article
Cardioprotection and Suppression of Fibrosis by Diverse Cancer and Non-Cancer Cell Lines in a Murine Model of Duchenne Muscular Dystrophy
by Laris Achlaug, Irina Langier Goncalves and Ami Aronheim
Int. J. Mol. Sci. 2024, 25(8), 4273; https://doi.org/10.3390/ijms25084273 - 12 Apr 2024
Viewed by 503
Abstract
The dynamic relationship between heart failure and cancer poses a dual challenge. While cardiac remodeling can promote cancer growth and metastasis, tumor development can ameliorate cardiac dysfunction and suppress fibrosis. However, the precise mechanism through which cancer influences the heart and fibrosis is [...] Read more.
The dynamic relationship between heart failure and cancer poses a dual challenge. While cardiac remodeling can promote cancer growth and metastasis, tumor development can ameliorate cardiac dysfunction and suppress fibrosis. However, the precise mechanism through which cancer influences the heart and fibrosis is yet to be uncovered. To further explore the interaction between heart failure and cancer, we used the MDX mouse model, which suffers from cardiac fibrosis and cardiac dysfunction. A previous study from our lab demonstrated that tumor growth improves cardiac dysfunction and dampens fibrosis in the heart and diaphragm muscles of MDX mice. We used breast Polyoma middle T (PyMT) and Lewis lung carcinoma (LLC) cancer cell lines that developed into large tumors. To explore whether the aggressiveness of the cancer cell line is crucial for the beneficial phenotype, we employed a PyMT breast cancer cell line lacking integrin β1, representing a less aggressive cell line compared to the original PyMT cells. In addition, we examined immortalized and primary MEF cells. The injection of integrin β1 KO PyMT cancer cells and Mouse Embryo Fibroblasts cells (MEF) resulted in the improvement of cardiac function and decreased fibrosis in the heart, diaphragm, and skeletal muscles of MDX mice. Collectively, our data demonstrate that the cancer line aggressiveness as well as primary MEF cells are sufficient to impose the beneficial phenotype. These discoveries present potential novel clinical therapeutic approaches with beneficial outcome for patients with fibrotic diseases and cardiac dysfunction that do not require tumor growth. Full article
(This article belongs to the Special Issue Advances in Cardiovascular Remodeling)
Show Figures

Figure 1

14 pages, 312 KiB  
Article
Impact of rs1805127 and rs55742440 Variants on Atrial Remodeling in Hypertrophic Cardiomyopathy Patients with Atrial Fibrillation: A Romanian Cohort Study
by Nicoleta-Monica Popa-Fotea, Nicoleta Oprescu, Alexandru Scafa-Udriste and Miruna Mihaela Micheu
Int. J. Mol. Sci. 2023, 24(24), 17244; https://doi.org/10.3390/ijms242417244 - 08 Dec 2023
Viewed by 789
Abstract
Atrial fibrillation (AFib) is characterized by a complex genetic component. We aimed to investigate the association between variations in genes related to cardiac ion handling and AFib in a cohort of Romanian patients with hypertrophic cardiomyopathy (HCM). Forty-five unrelated probands with HCM were [...] Read more.
Atrial fibrillation (AFib) is characterized by a complex genetic component. We aimed to investigate the association between variations in genes related to cardiac ion handling and AFib in a cohort of Romanian patients with hypertrophic cardiomyopathy (HCM). Forty-five unrelated probands with HCM were genotyped by targeted next-generation sequencing (NGS) for 24 genes associated with cardiac ion homeostasis. Subsequently, the study cohort was divided into two groups based on the presence (AFib+) or absence (AFiB−) of AFib detected during ECG monitoring. We identified two polymorphisms (rs1805127 located in KCNE1 and rs55742440 located in SCN1B) linked to AFib susceptibility. In AFib+, rs1805127 was associated with increased indexed left atrial (LA) maximal volume (LAVmax) (58.42 ± 21 mL/m2 vs. 32.54 ± 6.47 mL/m2, p < 0.001) and impaired LA strain reservoir (LASr) (13.3 ± 7.5% vs. 24.4 ± 6.8%, p < 0.05) compared to those without respective variants. The rs55742440 allele was less frequent in patients with AFib+ (12 out of 25, 48%) compared to those without arrhythmia (15 out of 20, 75%, p = 0.05). Also, AFib+ rs55742440 carriers had significantly lower LAVmax compared to those who were genotype negative. Among patients with HCM and AFib+, the rs1805127 variant was accompanied by pronounced LA remodeling, whereas rs55742440’s presence was related to a milder LA enlargement. Full article
(This article belongs to the Special Issue Advances in Cardiovascular Remodeling)
Back to TopTop