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Cells
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New Insights into Vascular Biology in Health and Disease
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New Insights into Vascular Biology in Health and Disease

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

Deadline for manuscript submissions: 15 September 2025 | Viewed by 9802

Special Issue Editor

Dr. Bashir M. Rezk

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Guest Editor
Biology Unit, Department of Natural Sciences, Southern University at New Orleans, New Orleans, LA 70126, USA
Interests: experimental and cellular therapeutics; the mechanisms of cardiovascular and inflammatory diseases, including but not limited to atherosclerosis, cancer and vascular complications

Special Issue Information

Dear Colleagues,

Vascular biology is crucial for understanding the mechanisms behind vascular diseases in the context of cardiovascular conditions, atherosclerosis, and cancer, as well as developing effective treatments and preventive strategies. Hyperhomocysteinemia is considered to be a major risk factor for multiple diseases. These include, but are not limited to, cardiovascular disease, stroke, diabetes, obesity, hypertension, renal failure, cancer, dementia, Alzheimer's, osteoporosis, and neurological disorders. The progression of vascular diseases is a multifactorial process, including endothelial dysfunction, vascular smooth muscle cell apoptosis, proliferation, and migration from the media to the intima. Under physiological conditions, cell proliferation and apoptosis are balanced since cell death triggers cell migration and proliferation. However, in pathogenic conditions, a selective increase in cell proliferation induces hyperplasia, and a selective elevation of apoptosis leads to atrophy. Autophagy has emerged in recent years as a critical cellular survival mechanism for cell homeostasis and may play a protective role in atherosclerosis. In lipid-rich atherosclerotic areas, angiogenesis is often associated with inflammatory cells that play a role in plaque instability and rupture. Furthermore, neovascularization is a prominent feature in advanced human atherosclerotic plaques and cancer.

The objective of this Special Issue is to spotlight recent discoveries related to autophagy, hyperhomocyteinemia, alcohols, and galectins in the progression of vascular diseases and the effective therapeutic targets.

Dr. Bashir M. Rezk
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

  • vascular diseases
  • cardiovascular
  • cancer
  • hyperhomocyteinemia
  • endothelial dysfunction
  • vascular smooth muscle cell
  • autophagy
  • alcohol
  • galectins
  • angiogenesis
  • neovascularization

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Published Papers (4 papers)

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Research

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12 pages, 3236 KiB  
Article
Perivascular Adipocytes’ Adipogenesis Is Defined by Their Anatomical Location in the Descending Thoracic Aorta
by G. Andres Contreras, C. Javier Rendon, Alyssa Shadowens, Miguel Chirivi, David Salcedo-Tacuma, D. Adam Lauver and Stephanie W. Watts
Cells 2025, 14(8), 579; https://doi.org/10.3390/cells14080579 - 11 Apr 2025
Viewed by 368
Abstract
Cardiovascular diseases such as hypertension alter thoracic aorta structure. The role that the outer layer of the aorta, its perivascular adipose tissue (PVAT), plays in the pathogenesis of these alterations is poorly understood. In the descending thoracic aorta, PVAT is organized into three [...] Read more.
Cardiovascular diseases such as hypertension alter thoracic aorta structure. The role that the outer layer of the aorta, its perivascular adipose tissue (PVAT), plays in the pathogenesis of these alterations is poorly understood. In the descending thoracic aorta, PVAT is organized into three distinct strips: one located anterior to the aorta (AP) and two positioned laterally (LP). Genetic tracing indicates differences in the ontogeny of LP and AP, but the implications of these developmental differences and PVAT distribution on adipocyte development remain unknown. We hypothesize that the anatomical location of adipocyte progenitors influences their adipogenic potential and vasoactive functions. PVAT from LP and AP was collected from male SD rats at 10 wks of age (n = 7) to harvest adipocyte progenitors that were differentiated to adipocytes in adipogenic media. Adipogenesis was evaluated after induction and we performed next-generation RNA-seq on progenitors and adipocytes. We then employed Gene Set Enrichment Analysis for enrichment and network analyses. LP progenitors exhibited a 1.13-fold higher adipogenesis rate compared to those from AP. DEG analysis revealed LP had higher expression of adipogenic regulators and basal collagens Col4a2 and Col4a4. When challenged with angiotensin-II, adipocyte progenitors from LP maintained their adipogenic capacity and adipocytes from the same site maintained their secretion of adiponectin at higher rates than AP cells. However, treatment with a Piezo1 mechanoreceptor agonist reduced LP’s adipogenic capacity and diminished their adiponectin secretion. These findings highlight site-specific differences in adipogenic activity, extracellular matrix composition, and the secretion of the vasoactive adipokine adiponectin between the LP and AP PVAT strips of the thoracic aorta, suggesting potential functional distinctions in vascular health and disease. Full article
(This article belongs to the Special Issue New Insights into Vascular Biology in Health and Disease)
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16 pages, 7441 KiB  
Article
Inhibition of Vascular Smooth Muscle Cell Proliferation by ENPP1: The Role of CD73 and the Adenosine Signaling Axis
by Boris Tchernychev, Yvonne Nitschke, Di Chu, Caitlin Sullivan, Lisa Flaman, Kevin O’Brien, Jennifer Howe, Zhiliang Cheng, David Thompson, Daniel Ortiz, Frank Rutsch and Yves Sabbagh
Cells 2024, 13(13), 1128; https://doi.org/10.3390/cells13131128 - 29 Jun 2024
Cited by 2 | Viewed by 3088
Abstract
The Ectonucleotide Pyrophosphatase/Phosphodiesterase 1 (ENPP1) ectoenzyme regulates vascular intimal proliferation and mineralization of bone and soft tissues. ENPP1 variants cause Generalized Arterial Calcification of Infancy (GACI), a rare genetic disorder characterized by ectopic calcification, intimal proliferation, and stenosis of large- and medium-sized arteries. [...] Read more.
The Ectonucleotide Pyrophosphatase/Phosphodiesterase 1 (ENPP1) ectoenzyme regulates vascular intimal proliferation and mineralization of bone and soft tissues. ENPP1 variants cause Generalized Arterial Calcification of Infancy (GACI), a rare genetic disorder characterized by ectopic calcification, intimal proliferation, and stenosis of large- and medium-sized arteries. ENPP1 hydrolyzes extracellular ATP to pyrophosphate (PPi) and AMP. AMP is the precursor of adenosine, which has been implicated in the control of neointimal formation. Herein, we demonstrate that an ENPP1-Fc recombinant therapeutic inhibits proliferation of vascular smooth muscle cells (VSMCs) in vitro and in vivo. Addition of ENPP1 and ATP to cultured VSMCs generated AMP, which was metabolized to adenosine. It also significantly decreased cell proliferation. AMP or adenosine alone inhibited VSMC growth. Inhibition of ecto-5′-nucleotidase CD73 decreased adenosine accumulation and suppressed the anti-proliferative effects of ENPP1/ATP. Addition of AMP increased cAMP synthesis and phosphorylation of VASP at Ser157. This AMP-mediated cAMP increase was abrogated by CD73 inhibitors or by A2aR and A2bR antagonists. Ligation of the carotid artery promoted neointimal hyperplasia in wild-type mice, which was exacerbated in ENPP1-deficient ttw/ttw mice. Prophylactic or therapeutic treatments with ENPP1 significantly reduced intimal hyperplasia not only in ttw/ttw but also in wild-type mice. These findings provide the first insight into the mechanism of the anti-proliferative effect of ENPP1 and broaden its potential therapeutic applications beyond enzyme replacement therapy. Full article
(This article belongs to the Special Issue New Insights into Vascular Biology in Health and Disease)
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Review

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28 pages, 1999 KiB  
Review
Pathophysiology of Angiotensin II-Mediated Hypertension, Cardiac Hypertrophy, and Failure: A Perspective from Macrophages
by Kelly Carter, Eshan Shah, Jessica Waite, Dhruv Rana and Zhi-Qing Zhao
Cells 2024, 13(23), 2001; https://doi.org/10.3390/cells13232001 - 4 Dec 2024
Cited by 4 | Viewed by 1578
Abstract
Heart failure is a complex syndrome characterized by cardiac hypertrophy, fibrosis, and diastolic/systolic dysfunction. These changes share many pathological features with significant inflammatory responses in the myocardium. Among the various regulatory systems that impact on these heterogeneous pathological processes, angiotensin II (Ang II)-activated [...] Read more.
Heart failure is a complex syndrome characterized by cardiac hypertrophy, fibrosis, and diastolic/systolic dysfunction. These changes share many pathological features with significant inflammatory responses in the myocardium. Among the various regulatory systems that impact on these heterogeneous pathological processes, angiotensin II (Ang II)-activated macrophages play a pivotal role in the induction of subcellular defects and cardiac adverse remodeling during the progression of heart failure. Ang II stimulates macrophages via its AT1 receptor to release oxygen-free radicals, cytokines, chemokines, and other inflammatory mediators in the myocardium, and upregulates the expression of integrin adhesion molecules on both monocytes and endothelial cells, leading to monocyte-endothelial cell-cell interactions. The transendothelial migration of monocyte-derived macrophages exerts significant biological effects on the proliferation of fibroblasts, deposition of extracellular matrix proteins, induction of perivascular/interstitial fibrosis, and development of hypertension, cardiac hypertrophy and heart failure. Inhibition of macrophage activation using Ang II AT1 receptor antagonist or depletion of macrophages from the peripheral circulation has shown significant inhibitory effects on Ang II-induced vascular and myocardial injury. The purpose of this review is to discuss the current understanding in Ang II-induced maladaptive cardiac remodeling and dysfunction, particularly focusing on molecular signaling pathways involved in macrophages-mediated hypertension, cardiac hypertrophy, fibrosis, and failure. In addition, the challenges remained in translating these findings to the treatment of heart failure patients are also addressed. Full article
(This article belongs to the Special Issue New Insights into Vascular Biology in Health and Disease)
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24 pages, 3786 KiB  
Review
Exosomes in Vascular/Neurological Disorders and the Road Ahead
by Faisal A. Alzahrani, Yasir M. Riza, Thamir M. Eid, Reema Almotairi, Lea Scherschinski, Jessica Contreras, Muhammed Nadeem, Sylvia E. Perez, Sudhanshu P. Raikwar, Ruchira M. Jha, Mark C. Preul, Andrew F. Ducruet, Michael T. Lawton, Kanchan Bhatia, Naseem Akhter and Saif Ahmad
Cells 2024, 13(8), 670; https://doi.org/10.3390/cells13080670 - 12 Apr 2024
Cited by 5 | Viewed by 3877
Abstract
Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), stroke, and aneurysms, are characterized by the abnormal accumulation and aggregation of disease-causing proteins in the brain and spinal cord. Recent research suggests that proteins linked [...] Read more.
Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), stroke, and aneurysms, are characterized by the abnormal accumulation and aggregation of disease-causing proteins in the brain and spinal cord. Recent research suggests that proteins linked to these conditions can be secreted and transferred among cells using exosomes. The transmission of abnormal protein buildup and the gradual degeneration in the brains of impacted individuals might be supported by these exosomes. Furthermore, it has been reported that neuroprotective functions can also be attributed to exosomes in neurodegenerative diseases. The potential neuroprotective functions may play a role in preventing the formation of aggregates and abnormal accumulation of proteins associated with the disease. The present review summarizes the roles of exosomes in neurodegenerative diseases as well as elucidating their therapeutic potential in AD, PD, ALS, HD, stroke, and aneurysms. By elucidating these two aspects of exosomes, valuable insights into potential therapeutic targets for treating neurodegenerative diseases may be provided. Full article
(This article belongs to the Special Issue New Insights into Vascular Biology in Health and Disease)
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