Vascular Biology: From Molecular Mechanisms to Precision Therapies

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 20 October 2026 | Viewed by 1143

Special Issue Editor


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Guest Editor
1. Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, GA, USA
2. Charlie Norwood VA Medical Center, Augusta, GA, USA
Interests: endothelium; vascular biology; lung injury; diabetic retinopathy; blood–tissue barrier

Special Issue Information

Dear Colleagues,

I am pleased to invite you to contribute to this forthcoming Special Issue of Cells, aiming to highlight recent advances in our understanding of vascular biology and how fundamental discoveries are being translated into targeted and precision-based therapeutic strategies.

The vascular endothelium plays a central role in maintaining tissue homeostasis, regulating blood–tissue barriers, and orchestrating inflammatory and metabolic responses. Dysregulation of vascular signaling contributes to a wide range of pathologies, including cardiovascular disease, lung injury, retinopathy, and other microvascular complications. Rapid progress in molecular, cellular, and system-level approaches has opened new opportunities to identify actionable targets and develop innovative therapies.

We welcome original research articles and comprehensive reviews addressing topics including, but not limited to, endothelial signaling mechanisms, vascular inflammation, angiogenesis, barrier dysfunction, metabolic regulation of the vasculature, and translational or precision-medicine approaches to vascular disease. I hope you will consider contributing to this Special Issue and joining us in advancing the field of vascular biology. Please feel free to contact me with any questions regarding suitability or scope.

Dr. Payaningal R. Somanath
Guest Editor

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Keywords

  • angiogenesis
  • endothelium
  • vascular permeability
  • blood–tissue barrier
  • organ injury

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Published Papers (2 papers)

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Review

30 pages, 1817 KB  
Review
Structural and Signaling Mechanisms of Aortic Wall Failure in Heritable Thoracic Aortic Disease
by Norifumi Takeda, Hiroki Yagi, Takayuki Fujiwara, Hitomi Aono-Setoguchi, Ryo Inuzuka and Issei Komuro
Cells 2026, 15(10), 936; https://doi.org/10.3390/cells15100936 (registering DOI) - 19 May 2026
Abstract
Heritable thoracic aortic diseases (HTAD) are inherited conditions that increase the risk of thoracic aortic aneurysms, dissections, and premature aortic rupture. Advances in human genetics and experimental models have transformed our understanding of these disorders from a phenotype-based classification system to a mechanism-based [...] Read more.
Heritable thoracic aortic diseases (HTAD) are inherited conditions that increase the risk of thoracic aortic aneurysms, dissections, and premature aortic rupture. Advances in human genetics and experimental models have transformed our understanding of these disorders from a phenotype-based classification system to a mechanism-based view involving extracellular matrix (ECM) architecture, transforming growth factor-β (TGFβ) signaling, and vascular smooth muscle cell contractility. Marfan syndrome, Loeys–Dietz syndrome, and nonsyndromic HTAD demonstrate how genetic mutations can disrupt the components that stabilize the aortic wall. These pathogenic mechanisms influence matrix organization, intracellular signaling, and the contractile machinery within the mechanically stressed proximal aorta. In this review, we summarize current mechanistic insights into the major forms of HTAD and discuss how new molecular and cellular concepts could influence surveillance, genetic counseling, and genotype-guided therapeutic strategies. Full article
(This article belongs to the Special Issue Vascular Biology: From Molecular Mechanisms to Precision Therapies)
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Graphical abstract

32 pages, 2306 KB  
Review
Claudins in Retinal Disease: Beyond Barrier Integrity to Signaling and Therapy
by Mohamed S. Selim, S. Priya Narayanan and Payaningal R. Somanath
Cells 2026, 15(5), 417; https://doi.org/10.3390/cells15050417 - 27 Feb 2026
Cited by 1 | Viewed by 939
Abstract
The blood–retinal barrier (BRB) maintains neurovascular homeostasis by regulating solute and ion exchange between the retina and circulation. This selectivity depends on tight junctions (TJs), with claudin (Cldn) proteins forming the core structure that defines paracellular permeability. Distinct Cldn isoforms show cell-specific expression, [...] Read more.
The blood–retinal barrier (BRB) maintains neurovascular homeostasis by regulating solute and ion exchange between the retina and circulation. This selectivity depends on tight junctions (TJs), with claudin (Cldn) proteins forming the core structure that defines paracellular permeability. Distinct Cldn isoforms show cell-specific expression, with Cldn-5 predominating in the endothelial cells of the inner BRB and Cldn-19 is the signature Cldn in the retinal pigment epithelium forming the outer BRB. Disruption of these isoforms contributes to vascular leakage, inflammation, and neuronal loss across various ocular diseases. Cldn function in vascular homeostasis is multifaceted; barrier dysfunction does not always result from Cldn loss, as excessive expression or mislocalization, particularly of Cldn-5, can also impair BRB integrity. Cldns act as dynamic signaling hubs that respond to metabolic, oxidative, and mechanical stress and are regulated through VEGF, Wnt/β-catenin, and RhoA/ROCK pathways. This review summarizes current understanding of Cldn biology in retinal vascular regulation and highlights emerging therapeutic strategies aimed at stabilizing Cldn expression and junctional localization. Small molecules and blocking antibodies that enhance localization or prevent degradation are redefining barrier repair. Key questions remain regarding isoform specificity, inter-barrier communication, and systemic safety. Integrative omics and spatial imaging may reveal disease-specific Cldn signatures and guide molecular restoration of BRB integrity. Full article
(This article belongs to the Special Issue Vascular Biology: From Molecular Mechanisms to Precision Therapies)
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