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Biomedicines
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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: 28 February 2026 | Viewed by 2082

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 (3 papers)

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Research

23 pages, 7234 KB  
Article
Cold Exposure Exacerbates Cardiac Dysfunction in a Model of Heart Failure with Preserved Ejection Fraction in Male and Female C57Bl/6J Mice
by Sara-Ève Thibodeau, Marie-Lune Legros, Emylie-Ann Labbé, Élisabeth Walsh-Wilkinson, Audrey Morin-Grandmont, Sarra Beji, Marie Arsenault, Alexandre Caron and Jacques Couet
Biomedicines 2025, 13(8), 1900; https://doi.org/10.3390/biomedicines13081900 - 4 Aug 2025
Viewed by 393
Abstract
Background: Standard room temperature housing (~22 °C) represents a stress for laboratory mice, resulting in an increased metabolic rate, calorie consumption, heart rate, and catecholamine levels compared to thermoneutral conditions (29–32 °C). Using a recently established two-hit model of heart failure with [...] Read more.
Background: Standard room temperature housing (~22 °C) represents a stress for laboratory mice, resulting in an increased metabolic rate, calorie consumption, heart rate, and catecholamine levels compared to thermoneutral conditions (29–32 °C). Using a recently established two-hit model of heart failure with preserved ejection fraction (HFpEF) (Angiotensin II + High-fat diet for 28 days; MHS), we investigated how housing temperature modulates cardiac remodelling and function in male and female C57Bl/6J mice. Methods: Using the MHS mouse model, we investigated cardiac remodelling and function in 8-week-old C57BL/6J mice of both sexes housed at 10 °C, 22 °C, and 30 °C for four weeks. Control mice were analyzed in parallel. Before the MHS, the animals were allowed to acclimate for a week before the MHS started. Results: Mice housed at 10 °C consumed more food and had increased fat mass compared to those at 22 °C or 30 °C. This was accompanied by increased heart weight, stroke volume, heart rate, and cardiac output. Mice housed at 22 °C and 30 °C were similar for these cardiac parameters. Following MHS, mice at 10 °C and 22 °C developed marked cardiac hypertrophy, whereas thermoneutral housing attenuated this response and reduced left atrial enlargement. Cold-exposed females showed more diastolic dysfunction after MHS (increased E’ wave, E/E’, and isovolumetric relaxation time) than those at 22 °C or 30 °C. Ejection fraction and cardiac output declined significantly at 10 °C after MHS but were preserved at 22 °C and 30 °C in females. Conclusions: Cold housing exacerbates cardiac dysfunction in mice subjected to HFpEF-inducing stress, with pronounced effects in females. In contrast, thermoneutrality limits the cardiac hypertrophic response. Full article
(This article belongs to the Special Issue Advances in Cardiovascular Remodeling: Molecular Mechanisms and Therapeutic Targets)
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21 pages, 23163 KB  
Article
Hyaluronan-Binding Protein Promotes Fibroblast Transformation and Heart Failure by Modulating the STAT5A–MMP13 Pathway
by Hui Yan, Bing Huang, Bofang Zhang, Yunyao Li, Qiping Zhou, Ayipali Abudoureyimu, Guiqiu Cao and Hong Jiang
Biomedicines 2025, 13(6), 1302; https://doi.org/10.3390/biomedicines13061302 - 26 May 2025
Viewed by 523
Abstract
Background: Adverse cardiac remodeling drives heart failure progression, but the role of hyaluronan-binding protein (HYBID) in this process remains unclear. This study investigated the role of HYBID as a key profibrotic factor in the progression of adverse cardiac remodeling with a focus on [...] Read more.
Background: Adverse cardiac remodeling drives heart failure progression, but the role of hyaluronan-binding protein (HYBID) in this process remains unclear. This study investigated the role of HYBID as a key profibrotic factor in the progression of adverse cardiac remodeling with a focus on its functional impact on cardiac fibroblasts and underlying molecular mechanisms. Methods: RNA sequencing analysis was employed to identify differentially expressed genes in mouse ventricular tissue post-myocardial infarction (MI). Fibroblast-specific genetically modified mouse models (knockdown and overexpression) were generated using FSP1 promoter-driven adeno-associated viruses. Comprehensive histological and biochemical assessments were conducted both in vivo and in vitro to evaluate the effects of HYBID modulation on cardiac remodeling. Molecular docking and immunoprecipitation assays were utilized to elucidate the mechanistic interactions between HYBID and its downstream targets. Results: RNA sequencing revealed HYBID as a fibroblast-enriched protein significantly upregulated in myocardial tissue of MI mice. Fibroblast-specific knockdown of HYBID attenuated MI-induced fibroblast activation, improved cardiac function, and mitigated adverse cardiac remodeling. Conversely, HYBID overexpression exacerbated fibroblast activation and promoted cardiac remodeling. Mechanistically, HYBID was found to competitively bind to STAT5A, thereby inhibiting the anti-fibrotic effects of MMP13 and driving fibroblast activation and adverse remodeling post-MI. Conclusions: Our findings establish HYBID as a novel fibroblast-enriched regulator that exacerbates fibrosis and adverse cardiac remodeling following MI. By uncovering the HYBID–STAT5A–MMP13 axis as a critical signaling pathway, this study provides new insights into the molecular mechanisms underlying heart failure progression. Full article
(This article belongs to the Special Issue Advances in Cardiovascular Remodeling: Molecular Mechanisms and Therapeutic Targets)
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17 pages, 1026 KB  
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 722
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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