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Smooth Muscle and Endothelial Cells as Pharmacological Targets for Acute...
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Smooth Muscle and Endothelial Cells as Pharmacological Targets for Acute Oxidative Stress

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (25 May 2025) | Viewed by 4436

Special Issue Editor

Dr. Charles E. Norton

E-Mail Website
Guest Editor
Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65212, USA
Interests: pulmonary hypertension; apoptosis; microcirculation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Reactive oxygen species (ROS) play an important role in physiological cell signaling. However, excessive levels of ROS damage cells. Acute oxidative stress results from ischemia reperfusion injuries such as stroke, myocardial infarction, and vascular occlusion during surgery in addition to acute injuries such as traumatic brain injury. While great attention has been devoted to limiting damage from acute oxidative stress on the surrounding tissue, the development of strategies to limit smooth muscle and endothelial cell damage to maintain perfusion to the effected tissue is emerging as a promising therapeutic focus.

Damage to smooth muscle and endothelial cells can impair vasomotor control and result in cell death. Recent efforts have begun to evaluate how to ameliorate this damage. In this Special Issue, we seek to bring together research from experts in the field to highlight pharmacological targets to limit vascular cell damage in response to acute oxidative stress. I look forward to receiving your valuable contributions.

Dr. Charles E. Norton
Guest Editor

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 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

  • reactive oxygen species
  • oxidative stress
  • smooth muscle cells
  • endothelium
  • ischemia/reperfusion
  • stroke
  • myocardial infarction
  • traumatic brain injury

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Published Papers (4 papers)

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Research

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15 pages, 4324 KiB  
Article
Plasminogen Activation Inhibitor-1 Promotes Resilience to Acute Oxidative Stress in Cerebral Arteries from Females
by Safa and Charles E. Norton
Pharmaceuticals 2024, 17(9), 1210; https://doi.org/10.3390/ph17091210 - 14 Sep 2024
Viewed by 1204
Abstract
Plasminogen activation inhibitor-1 (PAI-1) plays a central role in thrombus formation leading to stroke; however, the contributions of PAI-1 to cellular damage in response to reactive oxygen species which are elevated during reperfusion are unknown. Given that PAI-1 can limit apoptosis, we hypothesized [...] Read more.
Plasminogen activation inhibitor-1 (PAI-1) plays a central role in thrombus formation leading to stroke; however, the contributions of PAI-1 to cellular damage in response to reactive oxygen species which are elevated during reperfusion are unknown. Given that PAI-1 can limit apoptosis, we hypothesized that PAI increases the resilience of cerebral arteries to H2O2 (200 µM). Cell death, mitochondrial membrane potential, and mitochondrial ROS production were evaluated in pressurized mouse posterior cerebral arteries from males and females. The effects of pharmacological and genetic inhibition of PAI-1 signaling were evaluated with the inhibitor PAI-039 (10 µM) and PAI-1 knockout mice, respectively. During exposure to H2O2, PCAs from male mice lacking PAI-1 had reduced mitochondrial depolarization and smooth muscle cell death, and PAI-039 increased EC death. In contrast, mitochondrial depolarization and cell death were augmented in female PCAs. With no effect of PAI-1 inhibition on resting mitochondrial ROS production, vessels from female PAI-1 knockout mice had increased mitochondrial ROS generation during H2O2 exposure. During acute exposure to oxidative stress, protein ablation of PAI-1 enhances cell death in posterior cerebral arteries from females while limiting cell death in males. These findings provide important considerations for blood flow restoration during stroke treatment. Full article
(This article belongs to the Special Issue Smooth Muscle and Endothelial Cells as Pharmacological Targets for Acute Oxidative Stress)
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Review

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21 pages, 905 KiB  
Review
Phenotyping the Use of Cangrelor in Percutaneous Coronary Interventions
by Nikolaos Pyrpyris, Kyriakos Dimitriadis, Konstantinos G. Kyriakoulis, Stergios Soulaidopoulos, Panagiotis Tsioufis, Aggelos Papanikolaou, Nikolaos G. Baikoussis, Alexios Antonopoulos, Konstantinos Aznaouridis and Konstantinos Tsioufis
Pharmaceuticals 2025, 18(3), 432; https://doi.org/10.3390/ph18030432 - 19 Mar 2025
Viewed by 548
Abstract
The use of antiplatelet agents is essential in percutaneous coronary interventions, both periprocedurally and in the post-interventional period. Procedural antiplatelet therapy, aiming to limit ischemic complications, is mostly administered with oral agents, including aspirin and P2Y12 inhibitors. However, there are several limitations in [...] Read more.
The use of antiplatelet agents is essential in percutaneous coronary interventions, both periprocedurally and in the post-interventional period. Procedural antiplatelet therapy, aiming to limit ischemic complications, is mostly administered with oral agents, including aspirin and P2Y12 inhibitors. However, there are several limitations in the use of oral P2Y12 inhibitors, including their difficult administration in patients presenting with cardiogenic shock and their relatively slower onset of action, leaving a significant period of the procedure with a suboptimal antiplatelet effect. These pitfalls could be avoided with the use of cangrelor, the only available intravenous P2Y12 inhibitor, which has a rapid onset and offset antiplatelet effect, as well as a favorable pharmacological profile. The use of cangrelor has been increasing in recent years, with several studies aiming to determine what the optimal patient phenotype to receive such treatment ultimately is and how its use could be adjunctive to oral P2Y12 inhibitors. Therefore, the aim of this review is to provide an overview of the pharmacological profile of cangrelor and an update regarding the clinical evidence supporting its use, as well as to discuss the optimal patient phenotype, related clinical algorithms, and future implications for larger implementation of this agent into everyday clinical practice. Full article
(This article belongs to the Special Issue Smooth Muscle and Endothelial Cells as Pharmacological Targets for Acute Oxidative Stress)
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27 pages, 5191 KiB  
Review
Harnessing Gasotransmitters to Combat Age-Related Oxidative Stress in Smooth Muscle and Endothelial Cells
by Constantin Munteanu, Anca Irina Galaction, Gelu Onose, Marius Turnea and Mariana Rotariu
Pharmaceuticals 2025, 18(3), 344; https://doi.org/10.3390/ph18030344 - 27 Feb 2025
Viewed by 779
Abstract
Age-related oxidative stress is a critical factor in vascular dysfunction, contributing to hypertension and atherosclerosis. Smooth muscle cells and endothelial cells are particularly susceptible to oxidative damage, which exacerbates vascular aging through cellular senescence, chronic inflammation, and arterial stiffness. Gasotransmitters—hydrogen sulfide (H2 [...] Read more.
Age-related oxidative stress is a critical factor in vascular dysfunction, contributing to hypertension and atherosclerosis. Smooth muscle cells and endothelial cells are particularly susceptible to oxidative damage, which exacerbates vascular aging through cellular senescence, chronic inflammation, and arterial stiffness. Gasotransmitters—hydrogen sulfide (H2S), nitric oxide (NO), and carbon monoxide (CO)—are emerging as promising therapeutic agents for counteracting these processes. This review synthesizes findings from recent studies focusing on the mechanisms by which H2S, NO, and CO influence vascular smooth muscle and endothelial cell function. Therapeutic strategies involving exogenous gasotransmitter delivery systems and combination therapies were analyzed. H2S enhances mitochondrial bioenergetics, scavenges ROS, and activates antioxidant pathways. NO improves endothelial function, promotes vasodilation, and inhibits platelet aggregation. CO exhibits cytoprotective and anti-inflammatory effects by modulating heme oxygenase activity and ROS production. In preclinical studies, gasotransmitter-releasing molecules (e.g., NaHS, SNAP, CORMs) and targeted delivery systems show significant promise. Synergistic effects with lifestyle modifications and antioxidant therapies further enhance their therapeutic potential. In conclusion, gasotransmitters hold significant promise as therapeutic agents to combat age-related oxidative stress in vascular cells. Their multifaceted mechanisms and innovative delivery approaches make them potential candidates for treating vascular dysfunction and promoting healthy vascular aging. Further research is needed to translate these findings into clinical applications. Full article
(This article belongs to the Special Issue Smooth Muscle and Endothelial Cells as Pharmacological Targets for Acute Oxidative Stress)
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20 pages, 1911 KiB  
Review
Dysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases
by Ricky Patil, Hui Wang, Matthew Kazaleh, Gorav Ailawadi and Morgan Salmon
Pharmaceuticals 2025, 18(1), 112; https://doi.org/10.3390/ph18010112 - 16 Jan 2025
Viewed by 1151
Abstract
Mitochondria dysfunction plays a central role in the development of vascular diseases as oxidative stress promotes alterations in mitochondrial morphology and function that contribute to disease progression. Redox imbalances can affect normal cellular processes including mitochondrial biogenesis, electrochemical equilibrium, and the regulation of [...] Read more.
Mitochondria dysfunction plays a central role in the development of vascular diseases as oxidative stress promotes alterations in mitochondrial morphology and function that contribute to disease progression. Redox imbalances can affect normal cellular processes including mitochondrial biogenesis, electrochemical equilibrium, and the regulation of mitochondrial DNA. In this review, we will discuss these imbalances and, in particular, the potential role of mitochondrial fusion, fission, biogenesis, and mitophagy in the context of vascular diseases and how the dysregulation of normal function might contribute to disease progression. We will also discuss potential implications of targeting mitochondrial regulation as therapeutic targets to treat vascular disease formation. Full article
(This article belongs to the Special Issue Smooth Muscle and Endothelial Cells as Pharmacological Targets for Acute Oxidative Stress)
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