Molecular and Cellular Basis of Atherosclerosis Development

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: closed (25 June 2024) | Viewed by 413

Special Issue Editor


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Guest Editor
Cardiovascular Medicine Department, School of Medicine, Stanford University, Stanford, CA, USA
Interests: atherosclerosis; cardiovascular; vascular remodeling

Special Issue Information

Dear Colleagues,

Atherosclerotic plaques develop when arteries respond to high lipid levels. Various artery cell types participate in this process, including endothelial cells, smooth muscle cells, and adventitial fibroblasts.

Understanding how these cells coordinate to form a well-structured plaque is critical to developing corresponding therapeutics for atherosclerosis.

The aim of this Special Issue is to present the most recent progresses of vascular responses to atherosclerosis, which will help unravel potential therapeutic approaches. Therefore, we are pleased to invite you to submit an article or review focusing on the following topics:

  1.  Microenvironment remodeling of atherosclerotic plaques involving extracellular matrix, inflammation markers, and immune cells;
  2.  Lineage tracing mouse models and smooth muscle cell-specific perturbation of genes in these mouse models to understand their function in atherosclerosis;
  3.  Lineage tracing mouse models and endothelial cell-specific perturbation of genes in these mouse models to understand their function in atherosclerosis;
  4.  Lineage tracing mouse models and immune cell-specific perturbation of genes in these mouse models to understand their function in atherosclerosis;
  5.  Lineage tracing mouse models and adventitial fibroblast-specific perturbation of genes in these mouse models to understand their function in atherosclerosis;
  6.  Genetics risks and corresponding genes revealed by GWAS in coronary artery disease;
  7.  Summary of molecular pathways/mechanisms that were carried into current/ongoing treatments for coronary artery diseases.

Dr. Wenduo Gu
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. Cells is an international peer-reviewed open access semimonthly 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

  • atherosclerosis
  • endothelial cells
  • smooth muscle cells
  • adventitial fibroblasts
  • coronary artery diseases

Published Papers (1 paper)

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Research

15 pages, 11131 KiB  
Article
Paired Transcriptomic Analyses of Atheromatous and Control Vessels Reveal Novel Autophagy and Immunoregulatory Genes in Peripheral Artery Disease
by Praveen Machiraju, Rajesh Srinivas, Ramaraj Kannan, Robbie George, Stephane Heymans, Rupak Mukhopadhyay and Arkasubhra Ghosh
Cells 2024, 13(15), 1269; https://doi.org/10.3390/cells13151269 (registering DOI) - 28 Jul 2024
Abstract
Peripheral artery disease (PAD), a significant health burden worldwide, affects lower extremities due to atherosclerosis in peripheral vessels. Although the mechanisms of PAD have been well studied, the molecular milieu of the plaques localized within peripheral arteries are not well understood. Thus, to [...] Read more.
Peripheral artery disease (PAD), a significant health burden worldwide, affects lower extremities due to atherosclerosis in peripheral vessels. Although the mechanisms of PAD have been well studied, the molecular milieu of the plaques localized within peripheral arteries are not well understood. Thus, to identify PAD-lesion-specific gene expression profiles precluding genetic, environmental, and dietary biases, we studied the transcriptomic profile of nine plaque tissues normalized to non-plaque tissues from the same donors. A total of 296 upregulated genes, 274 downregulated genes, and 186 non-coding RNAs were identified. STAG1, SPCC3, FOXQ1, and E2F3 were key downregulated genes, and CD93 was the top upregulated gene. Autophagosome assembly, cellular response to UV, cytoskeletal organization, TCR signaling, and phosphatase activity were the key dysregulated pathways identified. Telomerase regulation and autophagy were identified as novel interacting pathways using network analysis. The plaque tissue was predominantly composed of immune cells and dedifferentiated cell populations indicated by cell-specific marker-imputed gene expression analysis. This study identifies novel genes, non-coding RNAs, associated regulatory pathways, and the cell composition of the plaque tissue in PAD patients. The autophagy and immunoregulatory genes may drive novel mechanisms, resulting in atheroma. These novel interacting networks and genes have potential for PAD-specific therapeutic applications. Full article
(This article belongs to the Special Issue Molecular and Cellular Basis of Atherosclerosis Development)
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