Recent Advances in Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases: 2nd Edition

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

Deadline for manuscript submissions: 31 July 2025 | Viewed by 12005

Special Issue Editor


E-Mail Website
Guest Editor
Department of Pathophysiology and Pharmacology, Institute of Cellular Biology and Pathology 'Nicolae Simionescu' of Romanian Academy, 8, BP Hasdeu Street, P.O. Box 35-14, 050568 Bucharest, Romania
Interests: cardiovascular disease; atherosclerosis; diabetes; obesity; inflammation; vascular dysfunction; biomarkers; therapies; extracellular vesicles; microvesicles; microRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular and metabolic diseases are disorders affecting the heart, blood vessels, as well as chemical processes within the body. They are the result of disturbances in genetic, environmental, and socioeconomic factors and cause a high number of deaths worldwide. The early detection of cardiovascular and metabolic diseases and the elucidation of cellular and molecular mechanisms are fundamental in preventing, intervening with, and monitoring their progression.

The Special Issue on “Recent Advances in Cellular and Molecular Mechanisms of Cardiovascular and Metabolic Diseases: Volume 2” will embrace up-to-date overviews of cellular and molecular biomarkers and pathogenic signaling pathways as potential targets for the development of effective therapeutic and monitoring strategies for cardiovascular and metabolic diseases.

Therefore, this Special Issue will provide a comprehensive approach to the detection and investigation of cardiovascular complications derived from metabolic disorders, such as dyslipidemia and diabetes, with the aim of discovering new therapies that are expected to improve patients’ quality of life. In this way, the future of preventing and treating cardiovascular and metabolic diseases can be reshaped.

Various forms of manuscripts, including reviews, original research articles, communications, and commentaries, are welcomed.

Dr. Adriana Georgescu
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. 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

  • cardiovascular disease
  • dyslipidemia
  • diabetes
  • obesity
  • inflammation
  • oxidative stress
  • biomarkers
  • microRNA
  • extracellular vesicles
  • cardiopulmonary disease

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

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

Related Special Issue

Published Papers (6 papers)

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

Research

Jump to: Review, Other

29 pages, 8599 KiB  
Article
Efficacy of Fetal Wharton’s Jelly Mesenchymal Stem Cells-Derived Small Extracellular Vesicles in Metabolic Syndrome
by Illayaraja Krishnan, Magdalene Tan Mei Ling, Min Hwei Ng, Jia Xian Law, Mohd Rafizul Mohd Yusof, Thavachelvi Thangarajah, Zalina Mahmood, Nurul Izzati Uda Zahli, Shathiya Rajamanickam, Baskar Subramani and Yogeswaran Lokanathan
Biomolecules 2025, 15(1), 44; https://doi.org/10.3390/biom15010044 - 1 Jan 2025
Viewed by 2018
Abstract
Background/Objective: Metabolic syndrome (MetS) is characterized by abdominal obesity, increased blood pressure (BP), fasting blood glucose (FBG) and triglyceride levels, and reduced high-density lipoprotein (HDL) levels. This study aims to investigate the efficacy of the Wharton’s jelly mesenchymal stem cells (WJMSCs)-derived small extracellular [...] Read more.
Background/Objective: Metabolic syndrome (MetS) is characterized by abdominal obesity, increased blood pressure (BP), fasting blood glucose (FBG) and triglyceride levels, and reduced high-density lipoprotein (HDL) levels. This study aims to investigate the efficacy of the Wharton’s jelly mesenchymal stem cells (WJMSCs)-derived small extracellular vesicles’ (sEVs) preparations in managing MetS. Method: Twenty-four rats were fed with a high-fat and high-fructose diet to induce MetS for 16 weeks and randomized into three groups (n = 8/group): a MetS Control group treated with normal saline, MetS Low Dose (LD) group treated with a LD of sEVs preparations (3 × 109 particle/rat), and MetS High Dose (HD) group treated with a HD of sEVs preparations (9 × 109 particles/rat). The Control Non-Disease (ND) group was given a standard rat diet and autoclaved tap water with normal saline as treatment. Treatments were given via intravenous injection every three weeks for twelve weeks. Rats were assessed every six weeks for physical measurements, FBG, lipid profiles, CRP, leptin, adiponectin, and BP. Necropsy evaluation was performed on the lungs, liver, spleen, and kidney. Results: Significant reductions in FBG, triglycerides, BP, and increased HDL levels were observed in the treated groups compared to the control group. However, significant abdominal circumference (AC) improvement was not observed in the treated groups. Non-significant associations were found between fasting CRP, leptin, and adiponectin levels with MetS rats after treatment. In addition, sEVs preparations improved inflammation and hemorrhage in the lung and mineralisation in the renal of the treated group. Conclusions: Human fetal WJMSCs-derived sEVs preparations improve all the clusters of MetS in rats except AC and could be further explored as a treatment for MetS. Full article
Show Figures

Figure 1

18 pages, 3666 KiB  
Article
Integrated Single-Cell Analysis Revealed Novel Subpopulations of Foamy Macrophages in Human Atherosclerotic Plaques
by Yunrui Lu, Shuang Wu, Shiyu Zhu, Jian Shen, Chang Liu, Chaoyue Zhao, Sheng’an Su, Hong Ma, Meixiang Xiang and Yao Xie
Biomolecules 2024, 14(12), 1606; https://doi.org/10.3390/biom14121606 - 16 Dec 2024
Viewed by 1440
Abstract
Foam cell formation is a hallmark of atherosclerosis, yet the cellular complexity within foam cells in human plaques remains unexplored. Here, we integrate published single-cell RNA-sequencing, spatial transcriptomic, and chromatin accessibility sequencing datasets of human atherosclerotic lesions across eight distinct studies. Through this [...] Read more.
Foam cell formation is a hallmark of atherosclerosis, yet the cellular complexity within foam cells in human plaques remains unexplored. Here, we integrate published single-cell RNA-sequencing, spatial transcriptomic, and chromatin accessibility sequencing datasets of human atherosclerotic lesions across eight distinct studies. Through this large-scale integration of patient-derived information, we identified foamy macrophages enriched for genes characteristic of the foamy signature. We further re-clustered the foamy macrophages into five unique subsets with distinct potential functions: (i) pro-foamy macrophages, exhibiting relatively high inflammatory and adhesive properties; (ii) phagocytic foamy macrophages, specialized in efferocytosis; (iii) high-efflux foamy macrophages marked by high NR1H3 expression; (iv) mature foamy macrophages prone to programmed cell death; and (v) synthetic subset. Trajectory analysis elucidated a bifurcated differentiation cell fate from pro-foam macrophages toward either the programmed death (iv) or synthetic (v) phenotype. The existence of these foamy macrophage subsets was validated by immunostaining. Moreover, these foamy macrophage subsets exhibited strong potential ligand–receptor interactions. Finally, we conducted Mendelian randomization analyses to identify a possible causal relationship between key regulatory genes along the programmed death pathway in foamy macrophages and atherosclerotic diseases. This study provides a high-resolution map of foam cell diversity and a set of potential key regulatory genes in atherosclerotic plaques, offering novel insights into the multifaceted pathophysiology underlying human atherosclerosis. Full article
Show Figures

Figure 1

Review

Jump to: Research, Other

16 pages, 787 KiB  
Review
Thyroid Hormones and Metabolism Regulation: Which Role on Brown Adipose Tissue and Browning Process?
by Laura Sabatino and Cristina Vassalle
Biomolecules 2025, 15(3), 361; https://doi.org/10.3390/biom15030361 - 2 Mar 2025
Viewed by 1628
Abstract
Thyroid hormones (THs) are important modulators of many metabolic processes, being strictly associated with the control of energy balance, mainly through activities on the brain, white and brown adipose tissue, skeletal muscle, liver, and pancreas. In this review, the principal mechanisms of TH [...] Read more.
Thyroid hormones (THs) are important modulators of many metabolic processes, being strictly associated with the control of energy balance, mainly through activities on the brain, white and brown adipose tissue, skeletal muscle, liver, and pancreas. In this review, the principal mechanisms of TH regulation on metabolic processes will be discussed and THs’ relevance in metabolic disease progression will be evaluated, especially in the cardiovascular context and correlated diseases. Moreover, we will discuss THs’ regulatory role on metabolic events in white and brown adipose tissue, with a special focus on the process of “browning”, which consists of the gradual acquisition by white adipocytes of the physical and functional characteristics of brown adipocytes. The advancements in research on molecular mechanisms and proposed physiopathological relevance of this process will be discussed. Full article
Show Figures

Figure 1

26 pages, 2738 KiB  
Review
The Emerging Role of m6A and Programmed Cell Death in Cardiovascular Diseases
by Haixia Wang, Juanjuan Han, Hui Kong, Ce Ma and Xin-an Zhang
Biomolecules 2025, 15(2), 247; https://doi.org/10.3390/biom15020247 - 8 Feb 2025
Cited by 2 | Viewed by 1260
Abstract
N6-methyladenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNA (mRNA), significantly impacting its lifecycle through dynamic and reversible processes involving methyltransferase, demethylase, and binding proteins. These processes regulate mRNA stability, splicing, nuclear export, translation, and degradation. Programmed cell death [...] Read more.
N6-methyladenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNA (mRNA), significantly impacting its lifecycle through dynamic and reversible processes involving methyltransferase, demethylase, and binding proteins. These processes regulate mRNA stability, splicing, nuclear export, translation, and degradation. Programmed cell death (PCD), a tightly controlled process encompassing apoptosis, pyroptosis, ferroptosis, autophagy, and necroptosis, plays a crucial role in maintaining cellular homeostasis, tissue development, and function. Recently, m6A modification has emerged as a significant research area due to its role in regulating PCD and its implications in cardiovascular diseases (CVDs). In this review, we delve into the intricate relationship between various PCD types and m6A modification, emphasizing their pivotal roles in the initiation and progression of CVDs such as myocardial ischemia-reperfusion (I/R), atherosclerosis (AS), pulmonary hypertension (PH), cardiomyopathy, doxorubicin (Dox)-induced cardiotoxicity (DIC), heart failure (HF), and myocardial infarction (MI). Our findings underscore the potential of elucidating the roles of m6A and PCD in CVD to pave new pathways for prevention and treatment strategies. Full article
Show Figures

Figure 1

28 pages, 2627 KiB  
Review
Targeting PDGF/PDGFR Signaling Pathway by microRNA, lncRNA, and circRNA for Therapy of Vascular Diseases: A Narrow Review
by Chao-Nan Ma, Shan-Rui Shi, Xue-Ying Zhang, Guo-Song Xin, Xiang Zou, Wen-Lan Li and Shou-Dong Guo
Biomolecules 2024, 14(11), 1446; https://doi.org/10.3390/biom14111446 - 14 Nov 2024
Cited by 1 | Viewed by 2315
Abstract
Despite the significant progress in diagnostic and therapeutic strategies, vascular diseases, such as cardiovascular diseases (CVDs) and respiratory diseases, still cannot be successfully eliminated. Vascular cells play a key role in maintaining vascular homeostasis. Notably, a variety of cells produce and secrete platelet-derived [...] Read more.
Despite the significant progress in diagnostic and therapeutic strategies, vascular diseases, such as cardiovascular diseases (CVDs) and respiratory diseases, still cannot be successfully eliminated. Vascular cells play a key role in maintaining vascular homeostasis. Notably, a variety of cells produce and secrete platelet-derived growth factors (PDGFs), which promote mitosis and induce the division, proliferation, and migration of vascular cells including vascular smooth muscle cells (SMCs), aortic SMCs, endothelial cells, and airway SMCs. Therefore, PDGF/PDGR receptor signaling pathways play vital roles in regulating the homeostasis of blood vessels and the onset and development of CVDs, such as atherosclerosis, and respiratory diseases including asthma and pulmonary arterial hypertension. Recently, accumulating evidence has demonstrated that microRNA, long-chain non-coding RNA, and circular RNA are involved in the regulation of PDGF/PDGFR signaling pathways through competitive interactions with target mRNAs, contributing to the occurrence and development of the above-mentioned diseases. These novel findings are useful for laboratory research and clinical studies. The aim of this article is to conclude the recent progresses in this field, particular the mechanisms of action of these non-coding RNAs in regulating vascular remodeling, providing potential strategies for the diagnosis, prevention, and treatment of vascular-dysfunction-related diseases, particularly CVDs and respiratory diseases. Full article
Show Figures

Figure 1

Other

Jump to: Research, Review

35 pages, 6967 KiB  
Systematic Review
Molecular Pathways Linking High-Fat Diet and PM2.5 Exposure to Metabolically Abnormal Obesity: A Systematic Review and Meta-Analysis
by Sagrario Lobato, Víctor Manuel Salomón-Soto, Claudia Magaly Espinosa-Méndez, María Nancy Herrera-Moreno, Beatriz García-Solano, Ernestina Pérez-González, Facundo Comba-Marcó-del-Pont, Mireya Montesano-Villamil, Marco Antonio Mora-Ramírez, Claudia Mancilla-Simbro and Ramiro Álvarez-Valenzuela
Biomolecules 2024, 14(12), 1607; https://doi.org/10.3390/biom14121607 - 16 Dec 2024
Viewed by 2252
Abstract
Obesity, influenced by environmental pollutants, can lead to complex metabolic disruptions. This systematic review and meta-analysis examined the molecular mechanisms underlying metabolically abnormal obesity caused by exposure to a high-fat diet (HFD) and fine particulate matter (PM2.5). Following the PRISMA guidelines, [...] Read more.
Obesity, influenced by environmental pollutants, can lead to complex metabolic disruptions. This systematic review and meta-analysis examined the molecular mechanisms underlying metabolically abnormal obesity caused by exposure to a high-fat diet (HFD) and fine particulate matter (PM2.5). Following the PRISMA guidelines, articles from 2019 to 2024 were gathered from Scopus, Web of Science, and PubMed, and a random-effects meta-analysis was performed, along with subgroup analyses and pathway enrichment analyses. This study was registered in the Open Science Framework. Thirty-three articles, mainly case–control studies and murine models, were reviewed, and they revealed that combined exposure to HFD and PM2.5 resulted in the greatest weight gain (82.835 g, p = 0.048), alongside increases in high-density lipoproteins, insulin, and the superoxide dismutase. HFD enriched pathways linked to adipocytokine signaling in brown adipose tissue, while PM2.5 impacted genes associated with fat formation. Both exposures downregulated protein metabolism pathways in white adipose tissue and activated stress-response pathways in cardiac tissue. Peroxisome proliferator-activated receptor and AMP-activated protein kinase signaling pathways in the liver were enriched, influencing non-alcoholic fatty liver disease. These findings highlight that combined exposure to HFD and PM2.5 amplifies body weight gain, oxidative stress, and metabolic dysfunction, suggesting a synergistic interaction with significant implications for metabolic health. Full article
Show Figures

Figure 1

Back to TopTop