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Molecular Advances and Insights on Diagnosis, Prevention and Therapeutics of Cardiovascular Diseases

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Guest Editor
Centre of Marine Sciences (CCMAR), University of Algarve, Campus de Gambelas, 8005-139 Faro, Portugal
Interests: vitamin-K-dependent proteins (VKDPs); Gla-rich protein (GRP); pathological calcification; chronic inflammatory diseases; clinical, therapeutic, and biomolecular aspects of Vitamin K and VKDPs
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Centre of Marine Sciences (CCMAR), Campus de Gambelas, Universidade do Algarve, 8005-139 Faro, Portugal
Interests: Gla-rich protein (GRP); calcification-related chronic inflammatory diseases; cardiovascular calcification; pathological calcification–inflammation molecular crosstalk; VKDPs in inflammation; VKDPs biomarker and therapeutic potential; extracellular vesicles
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) comprising a group of disorders of the heart and blood vessels, including coronary heart disease, stroke, peripheral arterial, and aortic disease, are the leading cause of morbidity and mortality globally with high prevalence in our aging society. Atherosclerosis is the leading cause of CVDs and cardiovascular-related death worldwide. Numerous pathological processes and molecular factors have been implicated in the development and progression of atherosclerosis including inflammation, vascular calcification, endothelial dysfunction, and oxidative stress.

Cardiovascular calcification caused by the deposition of calcium mineral in the vascular tree represents an increased risk of cardiovascular events and is associated with several vascular disease processes, not only in the intima associated with atherosclerosis, but also in the media layer highly prevalent in chronic kidney disease (CKD) and diabetic patients, and in cardiac valves associated with calcific valvular diseases.

A better understanding of the pathophysiological and molecular mechanisms involved at the genesis of these complex set of diseases, with a particular emphasis on inflammation and calcification processes, will bring new opportunities to explore novel biomarkers and therapeutic targets for CVD.

We are pleased to invite you to submit to this Special Issue on “Molecular Advances and Insights on Diagnosis, Prevention and Therapeutics of Cardiovascular Diseases”.

We will welcome original or review articles. Research areas may include (but not be limited to) the following: biomarkers; therapeutic targets, oxidative stress; inflammation, pathological calcification, cardiovascular calcification, atherosclerosis, chronic kidney disease, diabetes; obesity; diet supplements.

This Special Issue will include novel knowledge on biomedical science and translational research in order to comprehensively study and bring novel insights on the molecular aspects, the pathophysiology, the prevention, and therapeutic alternatives for this complex set of multifactorial diseases.

Dr. Dina Costa Simes
Dr. Carla Viegas
Guest Editors

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • cardiovascular disease
  • cardiovascular calcification
  • inflammation
  • oxidative stress
  • atherosclerosis
  • chronic kidney disease
  • endothelial dysfunction

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Published Papers (2 papers)

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Research

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22 pages, 6103 KiB  
Article
Gla Rich Protein (GRP) Mediates Vascular Smooth Muscle Cell (VSMC) Osteogenic Differentiation, Extracellular Vesicle (EV) Calcification Propensity, and Immunomodulatory Properties
by Carla Viegas, Joana Carreira, Teresa M. Maia, Anjos L. Macedo, António P. Matos, José Neves and Dina Simes
Int. J. Mol. Sci. 2024, 25(22), 12406; https://doi.org/10.3390/ijms252212406 - 19 Nov 2024
Cited by 1 | Viewed by 1183
Abstract
Vascular calcification (VC) is a complex process involving vascular smooth muscle cell (VSMC) osteogenic differentiation, inflammation, and extracellular vesicle (EV) calcification and communication networks. Gla rich protein (GRP) is a calcification inhibitor involved in most of these processes. However, the molecular mechanism of [...] Read more.
Vascular calcification (VC) is a complex process involving vascular smooth muscle cell (VSMC) osteogenic differentiation, inflammation, and extracellular vesicle (EV) calcification and communication networks. Gla rich protein (GRP) is a calcification inhibitor involved in most of these processes. However, the molecular mechanism of GRP in VC and the specific characteristics, cargo, and functionality of calcifying EVs require further elucidation. Here, we use a combination of human ex vivo aortic fragments and primary vascular smooth muscle cell (VSMC) models to obtain new information on GRP function in VC and EVs released by VSMCs. We demonstrate that GRP inhibits VSMC osteogenic differentiation through downregulation of bone-related proteins and upregulation of mineralization inhibitors, with decreased mineral crystallinity in EVs deposited into the tissue extracellular matrix (ECM). EVs isolated by ultracentrifugation at 30K and 100K from the cell media (CM) and deposited in the ECM from control (CTR) and mineralizing (MM) VSMCs were biochemically, physically, and proteomically characterized. Four different EV populations were identified with shared markers commonly present in all EVs but with unique protein cargo and specific molecular profiles. Comparative proteomics identified several regulated proteins specifically loaded into MM EV populations associated with multiple processes involved in VC. Functional analysis demonstrated that 30K and 100K ECM-MM EVs with higher calcium and lower GRP levels induced macrophage inflammation. Our findings reinforce the functional relevance of GRP in multiple VC processes and suggest that ECM EVs released under calcification stress function as a new signaling axis on the calcification–inflammation cycle. Full article
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25 pages, 6147 KiB  
Review
The Gut–Heart Axis: Molecular Perspectives and Implications for Myocardial Infarction
by Katherine Rivera, Leticia Gonzalez, Liena Bravo, Laura Manjarres and Marcelo E. Andia
Int. J. Mol. Sci. 2024, 25(22), 12465; https://doi.org/10.3390/ijms252212465 - 20 Nov 2024
Cited by 3 | Viewed by 3025
Abstract
Myocardial infarction (MI) remains the leading cause of death globally, imposing a significant burden on healthcare systems and patients. The gut–heart axis, a bidirectional network connecting gut health to cardiovascular outcomes, has recently emerged as a critical factor in MI pathophysiology. Disruptions in [...] Read more.
Myocardial infarction (MI) remains the leading cause of death globally, imposing a significant burden on healthcare systems and patients. The gut–heart axis, a bidirectional network connecting gut health to cardiovascular outcomes, has recently emerged as a critical factor in MI pathophysiology. Disruptions in this axis, including gut dysbiosis and compromised intestinal barrier integrity, lead to systemic inflammation driven by gut-derived metabolites like lipopolysaccharides (LPSs) and trimethylamine N-oxide (TMAO), both of which exacerbate MI progression. In contrast, metabolites such as short-chain fatty acids (SCFAs) from a balanced microbiota exhibit protective effects against cardiac damage. This review examines the molecular mediators of the gut–heart axis, considering the role of factors like sex-specific hormones, aging, diet, physical activity, and alcohol consumption on gut health and MI outcomes. Additionally, we highlight therapeutic approaches, including dietary interventions, personalized probiotics, and exercise regimens. Addressing the gut–heart axis holds promise for reducing MI risk and improving recovery, positioning it as a novel target in cardiovascular therapy. Full article
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