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Cells
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Molecular Pathways and Potential Therapeutic Targets of Vascular Dysfunction
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Molecular Pathways and Potential Therapeutic Targets of Vascular Dysfunction

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

Deadline for manuscript submissions: 30 August 2025 | Viewed by 3239

Special Issue Editor

Dr. Kenia Pedrosa Nunes

E-Mail Website
Guest Editor
Department of Biomedical Engineering and Sciences, Florida Institute of Technology, Melbourne, FL 32901, USA
Interests: vascular dysfunction; protein homeostasis; diabetes; hypertension; DAMPS; low-grade inflammation; aging; ROS; arterial stiffness; erectile dysfunction; innate immunity; TLR4
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The vasculature is crucial in human homeostasis, and an intricate net of pathways and signaling molecules mediates its functionality. The players in this scenario are the endothelial and vascular smooth muscle cells lining the blood vessels. Disruption in the mechanisms driving these two cells’ functionality leads to vascular dysfunction, which is central to the origin and development of vascular damage. Vascular dysfunction encompasses an injured endothelium characterized by an imbalance between vasoconstrictor and vasodilatory factors, microvascular dysfunction, and large artery damage by remodeling and arterial stiffening.

Vascular dysfunction leading to damaged vessels affects the quality of life and remains the leading cause of disease burden worldwide. It is a hallmark of a multitude of pathological conditions, including diabetes, hypertension, pre-eclampsia, and coronary and cerebrovascular diseases. Yet, there is a lack of information about mitigating vascular damage, and many molecular pathways need further investigation. Likewise, many paradigms require discussion, such as the role of innate immune receptors in mediating vascular dysfunction or whether there is a link between arterial stiffness and vascular dysfunction. This Special Issue welcomes manuscripts focusing on any aspect of vascular dysfunction-associated molecular pathways to enhance scientific comprehension, mitigate vascular damage, and unveil new therapeutic avenues to treat this condition.

Dr. Kenia Pedrosa Nunes
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 dysfunction
  • endothelial dysfunction
  • vascular remodeling
  • arterial stiffness
  • vascular signaling
  • new vascular targets

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Published Papers (4 papers)

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Research

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26 pages, 3678 KiB  
Article
Opposite Roles of IL-32α Versus IL-32β/γ Isoforms in Promoting Monocyte-Derived Osteoblast/Osteoclast Differentiation and Vascular Calcification in People with HIV
by Hardik Ramani, Aurélie Cleret-Buhot, Mohamed Sylla, Rémi Bunet, Florent Bertrand, Marc-Messier Peet, Carl Chartrand-Lefebvre, Benoit Trottier, Réjean Thomas, Jean-Pierre Routy, Claude Fortin, Valérie Martel-Laferrière, Manel Sadouni, Guy Cloutier, Louise Allard, Jorge R. Kizer, Nicolas Chomont, Petronela Ancuta, David B. Hanna, Robert C. Kaplan, Mohammad-Ali Jenabian, Alan L. Landay, Madeleine Durand, Mohamed El-Far and Cécile L. Tremblayadd Show full author list remove Hide full author list
Cells 2025, 14(7), 481; https://doi.org/10.3390/cells14070481 - 22 Mar 2025
Viewed by 405
Abstract
People with HIV (PWH) have an increased risk of developing cardiovascular disease (CVD). Our recent data demonstrated that the multi-isoform proinflammatory cytokine IL-32 is upregulated in PWH and is associated with arterial stiffness and subclinical atherosclerosis. However, the mechanisms by which IL-32 contributes [...] Read more.
People with HIV (PWH) have an increased risk of developing cardiovascular disease (CVD). Our recent data demonstrated that the multi-isoform proinflammatory cytokine IL-32 is upregulated in PWH and is associated with arterial stiffness and subclinical atherosclerosis. However, the mechanisms by which IL-32 contributes to the pathogenesis of these diseases remain unclear. Here, we show that while the less expressed IL-32α isoform induces the differentiation of human classical monocytes into the calcium-resorbing osteoclast cells, the dominantly expressed isoforms IL-32β and IL-32γ suppress this function through the inhibition of TGF-β and induce the differentiation of monocytes into the calcium-depositing osteocalcin+ osteoblasts. These results aligned with the increase in plasma levels of osteoprotegerin, a biomarker of vascular calcification, and its association with the presence of coronary artery subclinical atherosclerosis and calcium score in PWH. These findings support a novel role for the proinflammatory cytokine IL-32 in the pathophysiology of CVD by increasing vascular calcification in PWH. Full article
(This article belongs to the Special Issue Molecular Pathways and Potential Therapeutic Targets of Vascular Dysfunction)
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15 pages, 1619 KiB  
Article
Blockade of HSP70 Improves Vascular Function in a Mouse Model of Type 2 Diabetes
by Valentina Ochoa Mendoza, Amanda Almeida de Oliveira and Kenia Pedrosa Nunes
Cells 2025, 14(6), 424; https://doi.org/10.3390/cells14060424 - 13 Mar 2025
Viewed by 552
Abstract
Type 2 diabetes (T2D) is a chronic disease that damages blood vessels and increases the risk of cardiovascular disease (CVD). Heat-shock protein 70 (HSP70), a family of chaperone proteins, has been recently reported as a key player in vascular reactivity that affects large [...] Read more.
Type 2 diabetes (T2D) is a chronic disease that damages blood vessels and increases the risk of cardiovascular disease (CVD). Heat-shock protein 70 (HSP70), a family of chaperone proteins, has been recently reported as a key player in vascular reactivity that affects large blood vessels like the aorta. Hyperglycemia, a hallmark of diabetes, correlates with the severity of vascular damage and circulating HSP70 levels. In diabetes, blood vessels often show impaired contractility, contributing to vascular dysfunction. However, HSP70’s specific role in T2D-related vascular contraction remains unclear. We hypothesized that blocking HSP70 would improve vascular function in a widely used diabetic mouse model (db/db). To test this, we measured both vascular intracellular and serum circulating HSP70 levels in control and diabetic male mice using immunofluorescence and Western blotting. We also examined the aorta’s contractile response using a wire myograph system, which measured the force produced in response to phenylephrine (PE), both with and without VER155008, a pharmacological inhibitor that targets the ATPase domain of HSP70, and after removing extracellular calcium. Our findings show that intracellular HSP70 (iHSP70) levels were similar in control and diabetic groups, while circulating HSP70 (eHSP70) levels were higher in the serum of diabetic mice, altering the iHSP70/eHSP70 ratio. Even though VER155008 attenuated both phases of the contractile curve in the diabetic and control groups, enhanced vasoconstriction to PE was only observed in the tonic phase of the curve in the db/db group, which was prevented by iHSP70 inhibition. This effect involved calcium mobilization, as both the maximal and total contraction forces to PE were restored in groups treated with VER155008. Additionally, internal calcium levels in aortic rings treated with VER155008 decreased, as observed in force generation upon calcium reintroduction, which was further corroborated using a biochemical calcium assay. In conclusion, our study demonstrates that blocking HSP70 improves vascular reactivity in the hyperglycemic state of T2D by restoring proper vascular contraction. Full article
(This article belongs to the Special Issue Molecular Pathways and Potential Therapeutic Targets of Vascular Dysfunction)
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18 pages, 5736 KiB  
Article
Acute Chikungunya Infection Induces Vascular Dysfunction by Directly Disrupting Redox Signaling in Endothelial Cells
by José Teles de Oliveira-Neto, Juliano de P. Souza, Daniel Rodrigues, Mirele R. Machado, Juliano V. Alves, Paula R. Barros, Alecsander F. Bressan, Josiane F. Silva, Tiago J. Costa, Rafael M. Costa, Daniella Bonaventura, Eurico de Arruda-Neto, Rita C. Tostes and Emiliana P. Abrão
Cells 2024, 13(21), 1770; https://doi.org/10.3390/cells13211770 - 25 Oct 2024
Cited by 1 | Viewed by 1410
Abstract
Chikungunya virus (CHIKV) infection is characterized by febrile illness, severe joint pain, myalgia, and cardiovascular complications. Given that CHIKV stimulates reactive oxygen species (ROS) and pro- and anti-inflammatory cytokines, events that disrupt vascular homeostasis, we hypothesized that CHIKV induces arterial dysfunction by directly [...] Read more.
Chikungunya virus (CHIKV) infection is characterized by febrile illness, severe joint pain, myalgia, and cardiovascular complications. Given that CHIKV stimulates reactive oxygen species (ROS) and pro- and anti-inflammatory cytokines, events that disrupt vascular homeostasis, we hypothesized that CHIKV induces arterial dysfunction by directly impacting redox-related mechanisms in vascular cells. Wild-type (WT) and iNOS knockout (iNOS−/−) mice were administered either CHIKV (1.0 × 106 PFU/µL) or Mock vehicle via the intracaudal route. In vivo, CHIKV infection induced vascular dysfunction (assessed by a wire myograph), decreased systolic blood pressure (tail-cuff plethysmography), increased IL-6 and IFN-γ, but not TNF-α levels (determined by ELISA), and increased protein content by Western blot. Marked contractile hyporesponsiveness to phenylephrine was observed 48 h post-infection, which was restored by endothelium removal. L-NAME, 1400W, Tiron, and iNOS gene deletion prevented phenylephrine hyporesponsiveness. CHIKV infection increased vascular nitrite concentration (Griess reaction) and superoxide anion (O2•−) generation (lucigenin chemiluminescence), and decreased hydrogen peroxide (H2O2, by Amplex Red) levels 48 h post-infection, alongside increased TBARS levels. In vitro, CHIKV infected endothelial cells (EA.hy926) and upregulated ICAM-1 and iNOS protein expression (determined by Western blot). These data support the conclusion that CHIKV-induced alterations in vascular ROS/NF-kB/iNOS/NO signaling potentially contribute to cardiovascular events associated with Chikungunya infection. Full article
(This article belongs to the Special Issue Molecular Pathways and Potential Therapeutic Targets of Vascular Dysfunction)
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Review

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24 pages, 1380 KiB  
Review
The Role of Oxidative Stress and Inflammation in the Pathogenesis and Treatment of Vascular Dementia
by Aseel Y. Altahrawi, Antonisamy William James and Zahoor A. Shah
Cells 2025, 14(8), 609; https://doi.org/10.3390/cells14080609 - 17 Apr 2025
Viewed by 225
Abstract
Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern. VaD can be caused by cerebral infarction or [...] Read more.
Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern. VaD can be caused by cerebral infarction or injury in critical brain regions, including the speech area of the dominant hemisphere or arcuate fasciculus of the dominant hemisphere, leading to notable cognitive impairment. Although the exact causes of dementia remain multifactorial and complex, oxidative stress (reactive oxygen species), neuroinflammation (TNFα, IL-6, and IL-1β), and inflammasomes are considered central mechanisms in its pathology. These conditions contribute to neuronal damage, synaptic dysfunction, and cognitive decline. Thus, antioxidants and anti-inflammatory agents have emerged as potential therapeutic targets in dementia. Recent studies emphasize that cerebrovascular disease plays a dual role: first, as a primary cause of cognitive impairment and then as a contributor to the manifestation of dementia driven by other factors, such as Alzheimer’s disease and other neurodegenerative conditions. This comprehensive review of VaD focuses on molecular mechanisms and their consequences. We provided up-to-date knowledge about epidemiology, pathophysiological mechanisms, and current therapeutic approaches for VaD. Full article
(This article belongs to the Special Issue Molecular Pathways and Potential Therapeutic Targets of Vascular Dysfunction)
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