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Biomedicines
Special Issues
Advances in Cardiovascular Remodeling: Molecular Mechanisms and Therapeutic Targets
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Advances in Cardiovascular Remodeling: Molecular Mechanisms and Therapeutic Targets

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 524

Special Issue Editor

Dr. Elena Kaschina

E-Mail Website
Guest Editor
Max Rubner Center (MRC) for Cardiovascular Metabolic Renal Research, Institute of Pharmacology, Charité – Universitätsmedizin, Berlin, Hessische Strasse 3-4, D-10115 Berlin, Germany
Interests: cardiac and vascular remodeling; renin–angiotensin–aldosterone system; extracellular matrix; proteolysis; matrix metalloproteinases; heart failure; aneurysm
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular remodeling is characterized by changes in the size, mass and geometry of the heart and vessels. While initial physiological remodeling is adaptive to metabolic and hemodynamic stimuli, adverse remodeling promotes the development of cardiovascular diseases, especially heart failure, malignant arrythmias and aneurysms. Despite the range of treatment options available, these diseases remain life-threatening.

Remodeling is a complex process that involves inflammation, extracellular matrix degradation, hypertrophy, fibrosis and neurohormonal activation. Several alterations in ageing, such as vascular senescence, reduced regeneration and angiogenesis, also contribute to pathological remodeling. In response to injury, different types of cells, receptors and transporters are activated to ameliorate dysfunctional tissue remodeling. However, the complex interplay between all these pathophysiological processes is not completely understood and it is therefore crucial to unravel the main mechanisms underlying tissue remodeling. This will enable the development of novel biologic agents that target pathways, novel diagnostic techniques and advanced treatment strategies.

In this Special Issue, we welcome the submission of original manuscripts and reviews that describe recent advances in pathophysiology, diagnostics, the molecular mechanisms of tissue remodeling and novel treatments that prevent or reverse cardiovascular remodeling.

Dr. Elena Kaschina
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. Biomedicines 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

  • cardiac remodeling
  • vascular remodeling
  • ageing
  • pathogenesis
  • molecular mechanisms
  • diagnostics
  • therapy

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Published Papers (1 paper)

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Research

17 pages, 1026 KiB  
Article
Elevated Macrophage Migration Inhibitory Factor 1 Is Associated with Left and Right Ventricular Systolic Dysfunction in Heart Failure with Reduced Ejection Fraction
by Timea Magdolna Szabo, Mihály Vass, Márta Germán-Salló, Attila Frigy and Előd Ernő Nagy
Biomedicines 2025, 13(5), 1087; https://doi.org/10.3390/biomedicines13051087 - 30 Apr 2025
Viewed by 219
Abstract
Background/Objectives: Low-grade systemic inflammation, characteristic of heart failure (HF), is a nonspecific inflammatory syndrome that affects the entire body. Macrophage migration inhibitory factor 1 (MIF-1) is a pro-inflammatory cytokine, a key mediator of the innate immune response, and may serve as a [...] Read more.
Background/Objectives: Low-grade systemic inflammation, characteristic of heart failure (HF), is a nonspecific inflammatory syndrome that affects the entire body. Macrophage migration inhibitory factor 1 (MIF-1) is a pro-inflammatory cytokine, a key mediator of the innate immune response, and may serve as a potential biomarker of monocyte homing and activation in HF with reduced and mildly reduced ejection fraction (HFrEF, HFmrEF). Methods: We evaluated 70 hemodynamically stable patients with left ventricular EF (LVEF) < 50% by means of echocardiography and blood sampling. Results: We report significant correlations between MIF-1, LVEF (r = −0.33, p = 0.005), LV global longitudinal strain (LVGLS, r = 0.41, p = 0.0004), and tricuspid annular plane systolic excursion (TAPSE, r = −0.37, p = 0.001). MIF-1 levels in HFrEF patients were relatively higher, but not significantly different from those observed in HFmrEF. MIF-1 showed significant associations with TAPSE to systolic pulmonary artery pressure ratio (TAPSE/sPAP, p < 0.0001). Also, patients with TAPSE/sPAP < 0.40 mm/mmHg had significantly higher levels of MIF-1 (p = 0.009). Moreover, ischemic cardiomyopathy (ICM) was more frequent in patients with MIF-1 concentrations above 520 pg/mL (57.1% MIF-1hi vs. 28.6% MIF-1lo, p = 0.029). In terms of congestion, MIF-1 showed significant associations with the presence of peripheral edema (p = 0.007), but none was found with self-reported dyspnea (p = 0.307) and New York Heart Association (NYHA) class (p = 0.486). Also, no relationship was reported with N-terminal pro-B-type natriuretic peptide concentrations (NT-proBNP, r = 0.14, p = 0.263). However, the six-minute walk distance was greater in individuals in the MIF-1lo group when compared to those in the MIF-1hi group (404.0 ± 127.4 vs. 324.8 ± 124.1 m, p = 0.010). Conclusions: Beyond identifying inflammatory biomarkers related to disease severity, linking MIF-1 to various pathophysiological mechanisms may highlight the active involvement of the monocyte-macrophage system in HF. This system holds notable significance in congestion-related conditions, acting as a major source of reactive oxygen species that perpetuate inflammation. Full article
(This article belongs to the Special Issue Advances in Cardiovascular Remodeling: Molecular Mechanisms and Therapeutic Targets)
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