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Biomolecules
Special Issues
Cellular and Molecular Mechanisms in Cardiopathy and Therapeutic Strategies
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Cellular and Molecular Mechanisms in Cardiopathy and Therapeutic Strategies

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 January 2026 | Viewed by 1802

Special Issue Editors

Dr. Ying-Hsi Lin

E-Mail Website
Guest Editor
Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Medical School, Singapore, Singapore
Interests: cardiac physiology; cardiomyopathy; muscle mechanics; diastolic heart failures; mitochondrial biology
Special Issues, Collections and Topics in MDPI journals
Dr. Shengjie Lu

E-Mail Website
Guest Editor
National Heart Centre Singapore, Singapore 169609, Singapore
Interests: drug delivery; bioengineering; biomacromolecule and tissue engineering; cardiac medical device; nanomedicine and cardiac-targeting therapy

Special Issue Information

Dear Colleagues,

Cardiovascular disease (CVD), specifically heart failure (HF), is the leading cause of death globally and imposes a significant economic burden on the heartcare system. Despite current advances in the standard of care, the risk of death and the rehospitalization of HF patients remain unacceptably high. Notably, different forms of cardiopathies, defined as any sort of cardiac disease caused by maladaptive cardiac remodelling, impaired myocardial mechanics, and/or energetics, are often exposed along with the onset of HF symptoms and could act as potential targets to limit HF progression. Current treatments for cardiopathy include lifestyle changes, medications, and surgical or implantable devices, and with the advance in genome engineering, gene correction therapy for cardiomyopathy becomes promising. The primary objective of this Special Issue is to clarify our current understanding of the underlying mechanisms responsible for cardiopathy, preferably at cellular and molecular levels, that leads to HF and to explore the therapeutic strategies across interdisciplinary fields of biochemistry, biology, and engineering. We eagerly anticipate receiving your submissions and look forward to compiling an informative and insightful collection of articles.

Dr. Ying-Hsi Lin
Dr. Shengjie Lu
Guest Editors

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. Biomolecules 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 2700 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
  • cardiac remodelling
  • contractile dysfunction
  • bioenergetics
  • gene replacement or editing

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Published Papers (3 papers)

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Research

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13 pages, 8923 KB  
Article
Supercomplex Restructuring in Heart Mitochondria of COX7A1-Deficient Mice
by Lauren Pavelich, Lucynda Pham, Paul Stemmer, Icksoo Lee, Lawrence I. Grossman, Maik Hüttemann and Tasnim Arroum
Biomolecules 2025, 15(9), 1209; https://doi.org/10.3390/biom15091209 - 22 Aug 2025
Viewed by 190
Abstract
The role of electron transport chain supercomplexes and factors that regulate their composition in a tissue- and species-specific manner are not fully understood. Tissue-specific isoforms have been reported for cytochrome c oxidase (COX), which may contribute to such regulation. Therefore, we here investigated [...] Read more.
The role of electron transport chain supercomplexes and factors that regulate their composition in a tissue- and species-specific manner are not fully understood. Tissue-specific isoforms have been reported for cytochrome c oxidase (COX), which may contribute to such regulation. Therefore, we here investigated COX activity and structural organization in wild-type (WT) and COX7A1 knockout (KO) mice, which lack the heart/skeletal muscle isoform of COX subunit VIIa. COX7A1 KO mice showed a 30% reduction in total COX activity in the heart. Although the activity of COX in the monomers and I+III2+IVn supercomplexes (SCs) remained unchanged, a marked reduction in COX dimers and unknown COX-containing species IVx and IVy contributed to the overall reduction in COX activity. Furthermore, we observed that COX7A2 substituted for COX7A1 in COX monomers, dimers, and all COX-containing SCs in the KO mice, indicating a compensatory mechanism to preserve COX functionality. Collectively, these results suggest that COX7A1 plays an important role in maintaining structural stability; however, they also suggest that loss of COX7A1 is compensated by its replacement with COX7A2. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Cardiopathy and Therapeutic Strategies)
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Review

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21 pages, 1786 KB  
Review
Aortic Stiffness and Alzheimer’s Disease: The Medin Connection
by Filippos Triposkiadis, Andrew Xanthopoulos, Harisios Boudoulas and Dirk L. Brutsaert
Biomolecules 2025, 15(8), 1148; https://doi.org/10.3390/biom15081148 - 8 Aug 2025
Viewed by 387
Abstract
Aging is associated with aortic stiffening (AoSt), a condition characterized by diminished aortic elasticity that predisposes individuals to cognitive decline, including Alzheimer’s disease (AD). Emerging evidence implicates medin, which is derived from milk fat globule-EGF factor 8 protein (MFG-E8), as a key link [...] Read more.
Aging is associated with aortic stiffening (AoSt), a condition characterized by diminished aortic elasticity that predisposes individuals to cognitive decline, including Alzheimer’s disease (AD). Emerging evidence implicates medin, which is derived from milk fat globule-EGF factor 8 protein (MFG-E8), as a key link between AoSt and AD. Medin aggregates into aortic medial amyloid (AMA), which is found in approximately 97% of Caucasian individuals aged 50 and above, contributing to vascular inflammation, calcification, and loss of arterial elasticity. These changes may promote hyperpulsatile cerebral blood flow and impair glymphatic clearance, resulting in increased deposition of neurotoxic proteins, such as amyloid-β (Aβ) and possibly medin, which colocalizes with vascular Aβ in the brain. Medin enhances Aβ aggregation, generating heterologous fibrils, and thereby contributes to cerebrovascular dysfunction and neuroinflammation. This interaction (cross-seeding) may deteriorate amyloid pathology in both the vasculature and the parenchyma in AD. Furthermore, medin per se causes endothelial dysfunction, increases oxidative stress, and activates glial cells, promoting the development of a pro-inflammatory environment that enhances cognitive decline. In this manuscript, we contend that medin might act as a bridge connecting the age-related increase in aortic stiffness to AD, and therefore, medin might present a novel therapeutic target within this context. This hypothesis deserves experimental and clinical validation. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Cardiopathy and Therapeutic Strategies)
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16 pages, 1138 KB  
Review
Cardiac Myosin Inhibitors in the Treatment of Hypertrophic Cardiomyopathy: Clinical Trials and Future Challenges
by Arnold Kukowka and Marek Droździk
Biomolecules 2025, 15(8), 1098; https://doi.org/10.3390/biom15081098 - 29 Jul 2025
Viewed by 707
Abstract
Hypertrophic cardiomyopathy (HCM) is a prevalent and often underdiagnosed genetic cardiac disorder characterized by left ventricular hypertrophy and, in many cases, dynamic left ventricular outflow tract obstruction (LVOTO). The development of cardiac myosin inhibitors (CMIs) represents an emerging therapeutic approach in the pharmacological [...] Read more.
Hypertrophic cardiomyopathy (HCM) is a prevalent and often underdiagnosed genetic cardiac disorder characterized by left ventricular hypertrophy and, in many cases, dynamic left ventricular outflow tract obstruction (LVOTO). The development of cardiac myosin inhibitors (CMIs) represents an emerging therapeutic approach in the pharmacological management of obstructive HCM (oHCM). This review offers an integrated and up-to-date synthesis of the cardiac myosin inhibitor class, with a focus on mavacamten, aficamten, and the broader landscape of emerging agents. It also highlights recent clinical trial outcomes, pharmacokinetic and pharmacogenetic considerations, and potential future directions in therapy. Furthermore, we incorporate the most recent data up to May 2025, including late-breaking trial results and real-world safety findings, aiming to provide clinicians with a practical and comprehensive perspective on this evolving drug class. A narrative review was conducted by systematically searching PubMed, Scopus, Google Scholar, and ClinicalTrials.gov for English-language articles and trials published between January 2016 and May 2025. Keywords included “cardiac myosin inhibitor”, mavacamten”, “aficamten”, “MYK-224”, and “hypertrophic cardiomyopathy.” Inclusion criteria encompassed clinical trials and comprehensive reviews specifically addressing CMIs in cardiac applications. CMIs such as mavacamten and aficamten have demonstrated significant clinical benefits in reducing LVOT gradients, improving exercise capacity, and alleviating symptoms in patients with oHCM. Mavacamten is currently approved for clinical use, while aficamten is in advanced regulatory review. Comparative data suggest potential advantages of aficamten in the onset of action, pharmacokinetic profile, and tolerability. Emerging evidence supports the exploration of CMIs in pediatric populations, heart failure with preserved ejection fraction (HFpEF), and non-obstructive HCM (nHCM), although results are still preliminary. Cardiac myosin inhibitors offer a novel, pathophysiology-targeted approach to managing oHCM. While mavacamten has established efficacy, next-generation agents like aficamten may offer improved safety and versatility. Further long-term studies are needed to clarify their role across broader patient populations. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Cardiopathy and Therapeutic Strategies)
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