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Cells
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Cell Signalling in the Cardiovascular System
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Cell Signalling in the Cardiovascular System

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

Deadline for manuscript submissions: closed (1 June 2021) | Viewed by 13267

Special Issue Editor

Dr. Natalia López-Andrés

E-Mail Website
Guest Editor
Cardiovascular Translational Research, Navarrabiomed (Miguel Servet Foundation), Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), Pamplona, Spain
Interests: heart valve diseases; myocardial fibrosis and inflammation; heart failure

Special Issue Information

Dear Colleagues,

Heart valve disease (HVD) and heart failure (HF) are major health issues that are steadily increasing in prevalence in Western populations. In addition, ageing of the population will make incidence and prevalence of HVD and HF rise inexorably, unless effective preventive therapy is applied. No therapy targeting pathophysiological mechanisms, such as fibrosis or inflammation, is available for clinical use. The importance of fibrosis and inflammation in organ pathology and dysfunction appears to be increasingly relevant to a variety of distinct diseases. In particular, a number of different cardiovascular pathologies, including HVD and HF, seem to be caused by common fibrotic and inflammatory processes. With this scenario, analyzing new signaling pathways involved in fibrotic and inflammatory processes in the context of HVD and HF would have a great impact in society.

In this sense, the purpose of this Special Issue of Cells is to provide the reader with a collection of original research articles, reviews, and communications addressing the molecular and cellular basis of fibrosis and inflammation in HVD or HF. We aim to highlight the key involvement of cardiovascular cells in the pathophysiology of fibrosis and inflammation. Moreover, we aim to study molecules involved in the processes of fibroblast differentiation to myofibroblasts, collagen synthesis over degradation balance, collagen maturation, and/or valve cells pathophysiology.

We are looking forward to your contributions to this Special Issue.

Dr. Natalia López-Andrés
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

  • cardiovascular fibrosis
  • inflammation
  • heart failure
  • heart valve disease

Published Papers (3 papers)

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Research

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20 pages, 3492 KiB  
Article
High Glucose Treatment Limits Drosha Protein Expression and Alters AngiomiR Maturation in Microvascular Primary Endothelial Cells via an Mdm2-dependent Mechanism
by Brian Lam, Emmanuel Nwadozi, Tara L. Haas, Olivier Birot and Emilie Roudier
Cells 2021, 10(4), 742; https://doi.org/10.3390/cells10040742 - 27 Mar 2021
Cited by 5 | Viewed by 2550
Abstract
Diabetes promotes an angiostatic phenotype in the microvascular endothelium of skeletal muscle and skin. Angiogenesis-related microRNAs (angiomiRs) regulate angiogenesis through the translational repression of pro- and anti-angiogenic genes. The maturation of micro-RNA (miRs), including angiomiRs, requires the action of DROSHA and DICER proteins. [...] Read more.
Diabetes promotes an angiostatic phenotype in the microvascular endothelium of skeletal muscle and skin. Angiogenesis-related microRNAs (angiomiRs) regulate angiogenesis through the translational repression of pro- and anti-angiogenic genes. The maturation of micro-RNA (miRs), including angiomiRs, requires the action of DROSHA and DICER proteins. While hyperglycemia modifies the expression of angiomiRs, it is unknown whether high glucose conditions alter the maturation process of angiomiRs in dermal and skeletal muscle microvascular endothelial cells (MECs). Compared to 5 mM of glucose, high glucose condition (30 mM, 6–24 h) decreased DROSHA protein expression, without changing DROSHA mRNA, DICER mRNA, or DICER protein in primary dermal MECs. Despite DROSHA decreasing, high glucose enhanced the maturation and expression of one angiomiR, miR-15a, and downregulated an miR-15a target: Vascular Endothelial Growth Factor-A (VEGF-A). The high glucose condition increased Murine Double Minute-2 (MDM2) expression and MDM2-binding to DROSHA. Inhibition of MDM2 prevented the effects evoked by high glucose on DROSHA protein and miR-15a maturation in dermal MECs. In db/db mice, blood glucose was negatively correlated with the expression of skeletal muscle DROSHA protein, and high glucose decreased DROSHA protein in skeletal muscle MECs. Altogether, our results suggest that high glucose reduces DROSHA protein and enhances the maturation of the angiostatic miR-15a through a mechanism that requires MDM2 activity. Full article
(This article belongs to the Special Issue Cell Signalling in the Cardiovascular System)
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Review

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29 pages, 1902 KiB  
Review
Fibrosis, the Bad Actor in Cardiorenal Syndromes: Mechanisms Involved
by Beatriz Delgado-Valero, Victoria Cachofeiro and Ernesto Martínez-Martínez
Cells 2021, 10(7), 1824; https://doi.org/10.3390/cells10071824 - 19 Jul 2021
Cited by 14 | Viewed by 3784
Abstract
Cardiorenal syndrome is a term that defines the complex bidirectional nature of the interaction between cardiac and renal disease. It is well established that patients with kidney disease have higher incidence of cardiovascular comorbidities and that renal dysfunction is a significant threat to [...] Read more.
Cardiorenal syndrome is a term that defines the complex bidirectional nature of the interaction between cardiac and renal disease. It is well established that patients with kidney disease have higher incidence of cardiovascular comorbidities and that renal dysfunction is a significant threat to the prognosis of patients with cardiac disease. Fibrosis is a common characteristic of organ injury progression that has been proposed not only as a marker but also as an important driver of the pathophysiology of cardiorenal syndromes. Due to the relevance of fibrosis, its study might give insight into the mechanisms and targets that could potentially be modulated to prevent fibrosis development. The aim of this review was to summarize some of the pathophysiological pathways involved in the fibrotic damage seen in cardiorenal syndromes, such as inflammation, oxidative stress and endoplasmic reticulum stress, which are known to be triggers and mediators of fibrosis. Full article
(This article belongs to the Special Issue Cell Signalling in the Cardiovascular System)
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37 pages, 2377 KiB  
Review
Cardiac cAMP-PKA Signaling Compartmentalization in Myocardial Infarction
by Anne-Sophie Colombe and Guillaume Pidoux
Cells 2021, 10(4), 922; https://doi.org/10.3390/cells10040922 - 16 Apr 2021
Cited by 22 | Viewed by 6289
Abstract
Under physiological conditions, cAMP signaling plays a key role in the regulation of cardiac function. Activation of this intracellular signaling pathway mirrors cardiomyocyte adaptation to various extracellular stimuli. Extracellular ligand binding to seven-transmembrane receptors (also known as GPCRs) with G proteins and adenylyl [...] Read more.
Under physiological conditions, cAMP signaling plays a key role in the regulation of cardiac function. Activation of this intracellular signaling pathway mirrors cardiomyocyte adaptation to various extracellular stimuli. Extracellular ligand binding to seven-transmembrane receptors (also known as GPCRs) with G proteins and adenylyl cyclases (ACs) modulate the intracellular cAMP content. Subsequently, this second messenger triggers activation of specific intracellular downstream effectors that ensure a proper cellular response. Therefore, it is essential for the cell to keep the cAMP signaling highly regulated in space and time. The temporal regulation depends on the activity of ACs and phosphodiesterases. By scaffolding key components of the cAMP signaling machinery, A-kinase anchoring proteins (AKAPs) coordinate both the spatial and temporal regulation. Myocardial infarction is one of the major causes of death in industrialized countries and is characterized by a prolonged cardiac ischemia. This leads to irreversible cardiomyocyte death and impairs cardiac function. Regardless of its causes, a chronic activation of cardiac cAMP signaling is established to compensate this loss. While this adaptation is primarily beneficial for contractile function, it turns out, in the long run, to be deleterious. This review compiles current knowledge about cardiac cAMP compartmentalization under physiological conditions and post-myocardial infarction when it appears to be profoundly impaired. Full article
(This article belongs to the Special Issue Cell Signalling in the Cardiovascular System)
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