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Abnormal Regulation of Cellular Actions of Cardiovascular Factors

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 May 2023) | Viewed by 14986

Special Issue Editor


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Guest Editor
Depatment of Experimental Clinical Physiology, The Medical University of Warsaw, Warsaw, Poland
Interests: renin–angiotensin–aldosterone system; vasopressin; cytokines oxidative stress; reactive species; cardiovascular remodelling; myocardial infarction; hypertension

Special Issue Information

Dear Colleagues,

Numerous peptides synthetized by humans and animals have receptors in the heart and vessels and exert multiple regulatory effects on the cardiovascular system. They are generally known as cardiovascular peptides, because they are released during hemodynamic disturbances and directly act on the cells of the cardiovascular system. Cardiovascular peptides also exert regulatory effects on the water–electrolyte balance, metabolism and neural processes, and can indirectly tune the upregulation of the cardiovascular system. To date, attention has mainly been dedicated to the cardiovascular effects of angiotensin, vasopressin, and oxytocin; however, growing evidence is uncovering similar regulatory properties for several other peptide molecules. Experimental and clinical studies show that the action of the cardiovascular peptides may be altered under pathological conditions; however, the molecular mechanisms underlying these abnormalities are not satisfactorily elucidated. The main aim of the present Special Issue is to advance the knowledge of mechanisms modulating the cellular action of the cardiovascular peptides in various cells and tissues during physiological and pathological challenges. 

Dr. Ewa K Szczepanska-Sadowska
Guest Editor

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Keywords

  • angiotensin
  • autonomic nervous system
  • apelin
  • chemoreception
  • coronavirus
  • cytokine
  • diabetes
  • endothelin
  • glucagon
  • heart failure
  • hypertension
  • hypoxia
  • infection
  • insulin
  • natriuretic peptides
  • obesity
  • orexin
  • oxytocin
  • stress
  • vasopressin

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Published Papers (4 papers)

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Research

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12 pages, 1993 KiB  
Article
Impact of Heated Tobacco Products, E-Cigarettes, and Cigarettes on Inflammation and Endothelial Dysfunction
by Svenja Belkin, Julia Benthien, Paul Niklas Axt, Theresa Mohr, Kai Mortensen, Markus Weckmann, Daniel Drömann and Klaas Frederik Franzen
Int. J. Mol. Sci. 2023, 24(11), 9432; https://doi.org/10.3390/ijms24119432 - 29 May 2023
Cited by 10 | Viewed by 3764
Abstract
In addition to the market launch of heated tobacco products (HTPs) and the JUUL as well as the EVALI, they caused a widespread discussion on the risk reduction compared to a combustible cigarette. Furthermore, first data showed harmful effects on the cardiovascular system. [...] Read more.
In addition to the market launch of heated tobacco products (HTPs) and the JUUL as well as the EVALI, they caused a widespread discussion on the risk reduction compared to a combustible cigarette. Furthermore, first data showed harmful effects on the cardiovascular system. We, therefore, conducted investigations including a control group with a nicotine-free liquid. Forty active smokers were studied in two different approaches during and after consuming an HTP, a cigarette, a JUUL, or a typical electronic cigarette with or without nicotine in a partly double-blinded randomised, cross-over trial. Inflammation, endothelial dysfunction, and blood samples (full blood count, ELISA, multiplex immunoassay) were analysed, and arterial stiffness was measured. In addition to the cigarette, an increase in the white blood cell count but also in proinflammatory cytokines was shown for the various nicotine delivery systems. These correlated with the parameters of arterial vascular stiffness as a clinical parameter of endothelial dysfunction. It can be shown that even a single consumption of the different nicotine delivery system or cigarette leads to a significant inflammatory reaction followed by endothelial dysfunction and increased arterial stiffness causing cardiovascular disease. Inflammation, endothelial dysfunction, and arterial stiffness should be addressed in long-term observational studies. Full article
(This article belongs to the Special Issue Abnormal Regulation of Cellular Actions of Cardiovascular Factors)
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17 pages, 3933 KiB  
Article
Fetal Undernutrition Modifies Vascular RAS Balance Enhancing Oxidative Damage and Contributing to Remodeling
by Maria Sofia Vieira-Rocha, Pilar Rodriguez-Rodriguez, Mariana Ferreira-Duarte, Miguel Faria, Joana Beatriz Sousa, Manuela Morato, Silvia Magdalena Arribas and Carmen Diniz
Int. J. Mol. Sci. 2022, 23(3), 1233; https://doi.org/10.3390/ijms23031233 - 22 Jan 2022
Cited by 6 | Viewed by 2344
Abstract
Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers [...] Read more.
Fetal stress is known to increase susceptibility to cardiometabolic diseases and hypertension in adult age in a process known as fetal programming. This study investigated the relationship between vascular RAS, oxidative damage and remodeling in fetal programming. Six-month old Sprague-Dawley offspring from mothers that were fed ad libitum (CONTROL) or with 50% intake during the second half of gestation (maternal undernutrition, MUN) were used. qPCR or immunohistochemistry were used to obtain the expression of receptors and enzymes. Plasma levels of carbonyls were measured by spectrophotometry. In mesenteric arteries from MUN rats we detected an upregulation of ACE, ACE2, AT1 receptors and NADPH oxidase, and lower expression of AT2, Mas and MrgD receptors compared to CONTROL. Systolic and diastolic blood pressure and plasma levels of carbonyls were higher in MUN than in CONTROL. Vascular morphology evidenced an increased media/lumen ratio and adventitia/lumen ratio, and more connective tissue in MUN compared to CONTROL. In conclusion, fetal undernutrition indices RAS alterations and oxidative damage which may contribute to the remodeling of mesenteric arteries, and increase the risk of adverse cardiovascular events and hypertension. Full article
(This article belongs to the Special Issue Abnormal Regulation of Cellular Actions of Cardiovascular Factors)
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Review

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16 pages, 881 KiB  
Review
The Heart as a Target of Vasopressin and Other Cardiovascular Peptides in Health and Cardiovascular Diseases
by Ewa Szczepanska-Sadowska
Int. J. Mol. Sci. 2022, 23(22), 14414; https://doi.org/10.3390/ijms232214414 - 20 Nov 2022
Cited by 10 | Viewed by 5277
Abstract
The automatism of cardiac pacemaker cells, which is tuned, is regulated by the autonomic nervous system (ANS) and multiple endocrine and paracrine factors, including cardiovascular peptides. The cardiovascular peptides (CPs) form a group of essential paracrine factors affecting the function of the heart [...] Read more.
The automatism of cardiac pacemaker cells, which is tuned, is regulated by the autonomic nervous system (ANS) and multiple endocrine and paracrine factors, including cardiovascular peptides. The cardiovascular peptides (CPs) form a group of essential paracrine factors affecting the function of the heart and vessels. They may also be produced in other organs and penetrate to the heart via systemic circulation. The present review draws attention to the role of vasopressin (AVP) and some other cardiovascular peptides (angiotensins, oxytocin, cytokines) in the regulation of the cardiovascular system in health and cardiovascular diseases, especially in post-infarct heart failure, hypertension and cerebrovascular strokes. Vasopressin is synthesized mostly by the neuroendocrine cells of the hypothalamus. There is also evidence that it may be produced in the heart and lungs. The secretion of AVP and other CPs is markedly influenced by changes in blood volume and pressure, as well as by other disturbances, frequently occurring in cardiovascular diseases (hypoxia, pain, stress, inflammation). Myocardial infarction, hypertension and cardiovascular shock are associated with an increased secretion of AVP and altered responsiveness of the cardiovascular system to its action. The majority of experimental studies show that the administration of vasopressin during ventricular fibrillation and cardiac arrest improves resuscitation, however, the clinical studies do not present consisting results. Vasopressin cooperates with the autonomic nervous system (ANS), angiotensins, oxytocin and cytokines in the regulation of the cardiovascular system and its interaction with these regulators is altered during heart failure and hypertension. It is likely that the differences in interactions of AVP with ANS and other CPs have a significant impact on the responsiveness of the cardiovascular system to vasopressin in specific cardiovascular disorders. Full article
(This article belongs to the Special Issue Abnormal Regulation of Cellular Actions of Cardiovascular Factors)
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13 pages, 1369 KiB  
Review
Intersection of the Ubiquitin–Proteasome System with Oxidative Stress in Cardiovascular Disease
by Min Qiu, Jimei Chen, Xiaohong Li and Jian Zhuang
Int. J. Mol. Sci. 2022, 23(20), 12197; https://doi.org/10.3390/ijms232012197 - 13 Oct 2022
Cited by 10 | Viewed by 2628
Abstract
Cardiovascular diseases (CVDs) present a major social problem worldwide due to their high incidence and mortality rate. Many pathophysiological mechanisms are involved in CVDs, and oxidative stress plays a vital mediating role in most of these mechanisms. The ubiquitin–proteasome system (UPS) is the [...] Read more.
Cardiovascular diseases (CVDs) present a major social problem worldwide due to their high incidence and mortality rate. Many pathophysiological mechanisms are involved in CVDs, and oxidative stress plays a vital mediating role in most of these mechanisms. The ubiquitin–proteasome system (UPS) is the main machinery responsible for degrading cytosolic proteins in the repair system, which interacts with the mechanisms regulating endoplasmic reticulum homeostasis. Recent evidence also points to the role of UPS dysfunction in the development of CVDs. The UPS has been associated with oxidative stress and regulates reduction–oxidation homeostasis. However, the mechanisms underlying UPS-mediated oxidative stress’s contribution to CVDs are unclear, especially the role of these interactions at different disease stages. This review highlights the recent research progress on the roles of the UPS and oxidative stress, individually and in combination, in CVDs, focusing on the pathophysiology of key CVDs, including atherosclerosis, ischemia–reperfusion injury, cardiomyopathy, and heart failure. This synthesis provides new insight for continued research on the UPS–oxidative stress interaction, in turn suggesting novel targets for the treatment and prevention of CVDs. Full article
(This article belongs to the Special Issue Abnormal Regulation of Cellular Actions of Cardiovascular Factors)
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