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Biology
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Molecular Sciences in Cardiology and Vascular Disorders
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Molecular Sciences in Cardiology and Vascular Disorders

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 8174

Special Issue Editor

Dr. Ye Zeng

E-Mail Website
Guest Editor
Institute of Biomedical Engineering, West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, China
Interests: cardiovascular and cerebrovascular diseases; angiogenesis; glycocalyx; extracellular vesicles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to the Special Issue “Molecular Sciences in Cardiology and Vascular Disorders”. This issue sets forth in an enlightening exploration into the sophisticated realm of molecular biomedicine with an exclusive focus on cardiology and vascular disorders. By harnessing the principles of biology, chemistry, biomechanics, and medical science, this interdisciplinary field has considerably enriched our understanding of the complex operations and mechanisms underpinning the cardiovascular system.

Considering the global prevalence of cardiac and vascular diseases, the necessity for progression in this particular field is heightened. With the implementation of cutting-edge tools and methodologies hailing from molecular genetics, biochemistry, biophysics, and computational biology, cardiovascular research is experiencing a paradigm shift, revealing unprecedented insights, pioneering experimental models, and offering promising therapeutic approaches for these disorders.

The advances made in this vibrant field hold great promise, not only in expanding our understanding of cardiovascular pathophysiology, but crucially in driving forward the development methodology for combating ever-increasing cardiac and vascular disorders.

This Special Issue aims to serve as an exceptional platform for showcasing innovative research in the sphere of cardiac and vascular molecular sciences. We endeavor to stimulate thought-provoking discussions that expand our aggregated knowledge, incite innovative research avenues, and stimulate the creation of cutting-edge diagnostic mechanisms for cardiovascular diseases.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • molecular and genetic aspects of cardiovascular diseases;
  • biochemistry of cardiac and vascular systems;
  • biophysics in cardiovascular diseases;
  • computational modeling of cardiovascular functions;
  • stem cell and regeneration;
  • signaling in the cardiac and vascular systems;
  • pathophysiology of cardiovascular diseases.

We look forward to receiving your contributions.

Dr. Ye Zeng
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. Biology 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

  • cardiology
  • vascular disorders
  • atherosclerosis
  • microcirculation
  • biomechanics
  • biochemistry and molecular biology
  • cell biology
  • signaling pathway

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

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15 pages, 20759 KiB  
Article
Deletion of Interleukin-1β Converting Enzyme Alters Mouse Cardiac Structure and Function
by Gohar Azhar, Koichiro Nagano, Pankaj Patyal, Xiaomin Zhang, Ambika Verma and Jeanne Y. Wei
Biology 2024, 13(3), 172; https://doi.org/10.3390/biology13030172 - 7 Mar 2024
Cited by 1 | Viewed by 2017
Abstract
Interleukin-1β converting enzyme (ICE, caspase-1) is a thiol protease that cleaves the pro-inflammatory cytokine precursors of IL-1β and IL-18 into active forms. Given the association between caspase-1 and cardiovascular pathology, we analyzed the hearts of ICE knockout (ICE KO) mice to test the [...] Read more.
Interleukin-1β converting enzyme (ICE, caspase-1) is a thiol protease that cleaves the pro-inflammatory cytokine precursors of IL-1β and IL-18 into active forms. Given the association between caspase-1 and cardiovascular pathology, we analyzed the hearts of ICE knockout (ICE KO) mice to test the hypothesis that caspase-1 plays a significant role in cardiac morphology and function. We characterized the histological and functional changes in the hearts of ICE KO mice compared to the Wild type. The cardiomyocytes from the neonatal ICE KO mice showed an impaired response to oxidative stress. Subsequently, the hearts from the ICE KO mice were hypertrophied, with a significant increase in the left ventricular and septal wall thickness and a greater LV mass/body weight ratio. The ICE KO mice hearts exhibited irregular myofibril arrangements and disruption of the cristae in the mitochondrial structure. Proapoptotic proteins that were significantly increased in the hearts of ICE KO versus the Wild type included pErk, pJNK, p53, Fas, Bax, and caspase 3. Further, the antiapoptotic proteins Bag-1 and Bcl-2 are activated in ICE KO hearts. Functionally, there was an increase in the left ventricular epicardial diameter and volume in ICE KO. In conclusion, our findings support the important role of caspase-1 in maintaining cardiac health; specifically, a significant decrease in caspase-1 is detrimental to the cardiovascular system. Full article
(This article belongs to the Special Issue Molecular Sciences in Cardiology and Vascular Disorders)
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Review

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19 pages, 2161 KiB  
Review
Targeting Atherosclerosis via NEDD4L Signaling—A Review of the Current Literature
by Lucas Fornari Laurindo, Victória Dogani Rodrigues, Enzo Pereira de Lima, Beatriz Leme Boaro, Julia Maria Mendes Peloi, Raquel Cristina Ferraroni Sanches, Cláudia Rucco Penteado Detregiachi, Ricardo José Tofano, Maria Angelica Miglino, Katia Portero Sloan, Lance Alan Sloan and Sandra Maria Barbalho
Biology 2025, 14(3), 220; https://doi.org/10.3390/biology14030220 - 20 Feb 2025
Viewed by 927
Abstract
Cardiovascular diseases are the primary cause of mortality worldwide. In this scenario, atherosclerotic cardiovascular outcomes dominate since their incidence increases as populations grow and age. Atherosclerosis is a chronic inflammatory disease that affects arteries. Although its pathophysiology is heterogeneous, some genes are indissociably [...] Read more.
Cardiovascular diseases are the primary cause of mortality worldwide. In this scenario, atherosclerotic cardiovascular outcomes dominate since their incidence increases as populations grow and age. Atherosclerosis is a chronic inflammatory disease that affects arteries. Although its pathophysiology is heterogeneous, some genes are indissociably associated with its occurrence, and understanding their effects on the disease’s occurrence could undoubtedly define effective screening and treatment strategies. One such gene is NEDD4L. The NEDD4L gene is related to ubiquitin ligase enzyme activities. It is essential to regulate vascular inflammation, atherosclerosis plaque stability, endothelial and vascular smooth cell function, and lipid metabolism, particularly in controlling cholesterol levels. However, the evidence is dubious, and no review has yet synthesized the effects of targeting NEDD4L on atherosclerosis. Therefore, our review aims to fill this gap by analyzing the literature on NEDD4L concerning atherosclerosis occurrence. To achieve this goal, we performed a systematic literature search of reputable databases, including PubMed, Google Scholar, Web of Science, Scopus, and Embase. The inclusion criteria comprised peer-reviewed original studies using in vitro and animal models due to the unavailability of relevant clinical studies. Systematic reviews, meta-analyses, and articles that did not focus on the relationship between NEDD4L and atherosclerosis and those unrelated to this health condition were excluded. Studies not written in the English language were also excluded. The search strategy included studies from January 2000 to January 2025 in the final analysis to capture recent advancements. Following screening, five studies were included. Most of the included studies underscored NEDD4L’s role in increasing atherosclerosis plaque formation, but other studies indicated that stimulating NEDD4L may positively counter atherosclerosis plaque formation. Therefore, future research endeavors must address several limitations, which have been tentatively highlighted throughout the manuscript, for more informative research based on preclinical studies and to successfully translate the findings into clinical trials. Full article
(This article belongs to the Special Issue Molecular Sciences in Cardiology and Vascular Disorders)
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14 pages, 1643 KiB  
Review
Harnessing Mitochondrial Stress for Health and Disease: Opportunities and Challenges
by Yujia Sun, Linlu Jin, Yixue Qin, Zhi Ouyang, Jian Zhong and Ye Zeng
Biology 2024, 13(6), 394; https://doi.org/10.3390/biology13060394 - 29 May 2024
Cited by 3 | Viewed by 4370
Abstract
Mitochondria, essential organelles orchestrating cellular metabolism, have emerged as central players in various disease pathologies. Recent research has shed light on mitohormesis, a concept proposing an adaptive response of mitochondria to minor disturbances in homeostasis, offering novel therapeutic avenues for mitochondria-related diseases. This [...] Read more.
Mitochondria, essential organelles orchestrating cellular metabolism, have emerged as central players in various disease pathologies. Recent research has shed light on mitohormesis, a concept proposing an adaptive response of mitochondria to minor disturbances in homeostasis, offering novel therapeutic avenues for mitochondria-related diseases. This comprehensive review explores the concept of mitohormesis, elucidating its induction mechanisms and occurrence. Intracellular molecules like reactive oxygen species (ROS), calcium, mitochondrial unfolded proteins (UPRmt), and integrated stress response (ISR), along with external factors such as hydrogen sulfide (H2S), physical stimuli, and exercise, play pivotal roles in regulating mitohormesis. Based on the available evidence, we elucidate how mitohormesis maintains mitochondrial homeostasis through mechanisms like mitochondrial quality control and mitophagy. Furthermore, the regulatory role of mitohormesis in mitochondria-related diseases is discussed. By envisioning future applications, this review underscores the significance of mitohormesis as a potential therapeutic target, paving the way for innovative interventions in disease management. Full article
(This article belongs to the Special Issue Molecular Sciences in Cardiology and Vascular Disorders)
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