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Special Issue "Oxidative Stress in Hypertension: Mechanisms and Potential Pharmacological Targets"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: 30 June 2020.

Special Issue Editor

Prof. Anna Dikalova
E-Mail Website
Guest Editor
Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN 37232, USA
Interests: oxidative stress; endothelial dysfunction; systemic hypertension; mitochondrial dysfunction

Special Issue Information

Dear colleagues,

Hypertension represents a major risk factor for stroke, myocardial infarction, and heart failure, which cause one-third of deaths worldwide. Hypertension is a multifactorial disorder involving perturbations of the vasculature, kidney, and immune and central nervous systems. Despite treatment with multiple drugs, 37% of hypertensive patients remain hypertensive, likely due to mechanisms contributing to blood pressure elevation that are not affected by current treatments. Unraveling the underlying causes of vascular dysfunction is critical to improving disease burden. Metabolic disorders and oxidative stress contribute to the pathogenesis of vascular dysfunction and hypertension which are associated with mitochondrial dysfunction and altered cell redox signaling. Targeting specific sources of oxidative stress such as NADPH oxidases or mitochondrial metabolic functions can improve vascular function, reduce hypertension, and reduce morbidity and mortality associated with these pathological conditions.

In this Special Issue, we will discuss the novel mechanisms of oxidative stress, its role in metabolic dysregulation and inflammation, and describe the therapeutic potential of targeting specific oxidative stress and metabolic pathways to improve vascular function and reduce hypertension.

Prof. Anna Dikalova
Guest Editor

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • Essential hypertension
  • Pulmonary hypertension
  • Endothelial dysfunction
  • Vascular hypertrophy
  • Inflammation
  • Oxidative stress
  • Mitochondria
  • Metabolic conditions
  • Superoxide radical
  • Superoxide dismutase
  • Isolevuglandins
  • NADPH oxidase

Published Papers (3 papers)

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Research

Open AccessArticle
Chronic Cannabidiol Administration Fails to Diminish Blood Pressure in Rats with Primary and Secondary Hypertension Despite Its Effects on Cardiac and Plasma Endocannabinoid System, Oxidative Stress and Lipid Metabolism
Int. J. Mol. Sci. 2020, 21(4), 1295; https://doi.org/10.3390/ijms21041295 (registering DOI) - 14 Feb 2020
Abstract
We investigated the influence of cannabidiol (CBD) on blood pressure (BP) and heart rate (HR) in spontaneously (SHR) and deoxycorticosterone (DOCA-salt) hypertensive rats. Hypertension was connected with increases in cardiac and plasma markers of lipid peroxidation in both models, whereas cardiac endocannabinoid levels [...] Read more.
We investigated the influence of cannabidiol (CBD) on blood pressure (BP) and heart rate (HR) in spontaneously (SHR) and deoxycorticosterone (DOCA-salt) hypertensive rats. Hypertension was connected with increases in cardiac and plasma markers of lipid peroxidation in both models, whereas cardiac endocannabinoid levels decreased in SHR and increased in DOCA-salt. CBD (10 mg/kg once a day for 2 weeks) did not modify BP and HR in hypertension but counteracted pro-oxidant effects. Moreover, it decreased cardiac or plasma levels of anandamide, 2-arachidonoylglycerol and oleoyl ethanolamide in DOCA-salt and inhibited the activity of fatty acid amide hydrolase (FAAH) in both models. In the respective normotensive control rats, CBD increased lipid peroxidation, free fatty acid levels and FAAH activity. In conclusion, chronic CBD administration does not possess antihypertensive activity in a model of primary and secondary (DOCA-salt) hypertension, despite its antioxidant effect. The latter may be direct rather than based on the endocannabinoid system. The unexpected CBD-related increase in lipid peroxidation in normotensive controls may lead to untoward effects; thus, caution should be kept if CBD is used therapeutically. Full article
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Open AccessArticle
Conditioned Medium from Human Adipose-Derived Mesenchymal Stem Cell Culture Prevents UVB-Induced Skin Aging in Human Keratinocytes and Dermal Fibroblasts
Int. J. Mol. Sci. 2020, 21(1), 49; https://doi.org/10.3390/ijms21010049 - 19 Dec 2019
Abstract
Human adipose-derived mesenchymal stem cells-conditioned medium (ADSC-CM) contains cytokines and growth factors that can facilitate the regeneration and repair of various tissues and organs. In the present study, the protective activity of ADSC-CM treatment was investigated in UVB-irradiated human keratinocyte cell line HaCaTs [...] Read more.
Human adipose-derived mesenchymal stem cells-conditioned medium (ADSC-CM) contains cytokines and growth factors that can facilitate the regeneration and repair of various tissues and organs. In the present study, the protective activity of ADSC-CM treatment was investigated in UVB-irradiated human keratinocyte cell line HaCaTs and normal human dermal fibroblasts (NHDFs). It was found that ADSC-CM can modulate the expression of the signaling molecules in the early UVB responsive signaling pathways, including mitogen activated protein kinases (MAPKs), activator protein 1 (AP-1), and nuclear factor kappa B (NF-κB). In addition, ADSC-CM treatment could upregulate antioxidant response element (ARE) such as phase II gene heme oxygenase-1 (HO-1) and increase the expression of collagen synthesis enhancer gene transforming growth factor-β (TGF-β). The expression of matrix metalloproteinase-1 (MMP-1) and procollagen type I synthesis inhibitors such as interleukin-6 (IL-6) was also found to be suppressed upon ADSC-CM treatment. Taken together, our study illustrates the anti-photoaging activities of ADSC-CM in cell-based models. Full article
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Open AccessArticle
Protection of Male Rat Offspring against Hypertension Programmed by Prenatal Dexamethasone Administration and Postnatal High-Fat Diet with the Nrf2 Activator Dimethyl Fumarate during Pregnancy
Int. J. Mol. Sci. 2019, 20(16), 3957; https://doi.org/10.3390/ijms20163957 - 14 Aug 2019
Abstract
Hypertension can originate from early-life exposure to oxidative stress. As reported, dimethyl fumarate (DMF) activates nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and protects against oxidative stress damage. We examined whether maternal DMF therapy protects adult offspring against hypertension programmed by prenatal dexamethasone [...] Read more.
Hypertension can originate from early-life exposure to oxidative stress. As reported, dimethyl fumarate (DMF) activates nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and protects against oxidative stress damage. We examined whether maternal DMF therapy protects adult offspring against hypertension programmed by prenatal dexamethasone (DEX) and postnatal high-fat (HF) diet exposure. We examined male Sprague Dawley rat offspring at 4 months of age from five groups (n = 11–13/group): control, DEX (0.1mg/kg i.p. from gestational day 16 to 22), HF (D12331 diet from weaning to 16 weeks of age), DEX+HF, and DEX+HF+DMF (50mg/kg/day via gastric gavage for 3 weeks during pregnancy). Maternal DMF therapy prevented male offspring against hypertension programmed by combined DEX and HF exposures. The protective effects of maternal DMF include reduced oxidative stress, decreased plasma asymmetric dimethylarginine (ADMA) levels, downregulated the renin-angiotensin system (i.e. Ren, Agt, Ace, and Agtr1a), increased renal protein levels of certain nutrient-sensing signals, and promoted autophagy. In conclusion, maternal Nrf2 activation by DMF protects male adult offspring against hypertension programmed by combined DEX and HF exposures. Our results cast a new light on the therapeutic potential of targeting Nrf2 signaling pathway as reprogramming strategies to prevent programmed hypertension in children exposed to antenatal corticosteroids and postnatally excessive consumption of fat. Full article
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