ijms-logo

Journal Browser

Journal Browser

Molecular Mechanisms and Signalling Pathways in Cardiovascular Pathophysiology

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: 30 January 2025 | Viewed by 265

Special Issue Editor


E-Mail Website
Guest Editor
Centro de Investigaciones Cardiovasculares “Dr. Horacio E. Cingolani”, Facultad de Ciencias Médicas, Universidad Nacional de La Plata—CONICET, La Plata, Buenos Aires 1900, Argentina
Interests: arrhythmia; heart; vascular; signaling; cardiovascular disease; mechanism

Special Issue Information

Dear Colleagues,

As is well known, cardiovascular diseases are the leading cause of death worldwide. Understanding the pathophysiological processes that lead to the wide variety of these pathologies is essential to establishing the most appropriate treatments to combat them. In recent years, special interest has been gained in research into the subcellular processes associated with the pathophysiological particularity of each patient, with the aim of steering to more precise therapeutic strategies. This is why basic research into the cardiovascular pathophysiological intracellular signaling pathways and the molecular mechanisms involved in them is of crucial importance. Thus, this Special Issue welcomes articles that present new evidence that strengthens the knowledge of these pathophysiological mechanisms of the cardiovascular system, including cardiac and vascular excitation–contraction coupling dysfunction, endothelial damage, hypertension, heart failure, maladaptive hypertrophy, diabetic heart, and altered bioenergetics, among other mechanisms. In summary, this Special Issue aims to focus on both basic science and translational research to gain a better understanding of the pathophysiological mechanisms leading to cardiovascular diseases.

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

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • heart
  • vascular
  • signaling
  • cardiovascular disease
  • mechanism

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

13 pages, 5343 KiB  
Article
Activation of G Protein-Coupled Estrogen Receptor (GPER) Negatively Modulates Cardiac Excitation–Contraction Coupling (ECC) through the PI3K/NOS/NO Pathway
by Leandro A. Diaz-Zegarra, María S. Espejo, Alejandro M. Ibañez, Mónica E. Rando, Lucia E. Pagola, Verónica C. De Giusti and Ernesto A. Aiello
Int. J. Mol. Sci. 2024, 25(16), 8993; https://doi.org/10.3390/ijms25168993 - 19 Aug 2024
Viewed by 223
Abstract
The G-protein-coupled estrogen receptor (GPER) has been described to exert several cardioprotective effects. However, the exact mechanism involved in cardiac protection remains unclear. The aim of this study is to investigate the role of GPER activation on excitation–contraction coupling (ECC) and the possibility [...] Read more.
The G-protein-coupled estrogen receptor (GPER) has been described to exert several cardioprotective effects. However, the exact mechanism involved in cardiac protection remains unclear. The aim of this study is to investigate the role of GPER activation on excitation–contraction coupling (ECC) and the possibility that such effect participates in cardioprotection. The cardiac myocytes of male Wistar rats were isolated with a digestive buffer and loaded with Fura-2-AM for the measurement of intracellular calcium transient (CaT). Sarcomere shortening (SS) and L-type calcium current (ICaL) were also registered. The confocal technique was used to measure nitric oxide (NO) production in cells loaded with DAF-FM-diacetate. Cardiac myocytes exposed to 17-β-estradiol (E2, 10 nM) or G-1 (1 μM) for fifteen minutes decreased CaT, SS, and ICaL. These effects were prevented using G-36 (antagonist of GPER, 1 μM), L-Name (NO synthase -NOS- inhibitor, 100 nM), or wortmannin (phosphoinositide-3-kinase -PI3K- inhibitor, 100 nM). Moreover, G1 increased NO production, and this effect was abolished in the presence of wortmannin. We concluded that the selective activation of GPER with E2 or G1 in the isolated cardiac myocytes of male rats induced a negative inotropic effect due to the reduction in ICaL and the decrease in CaT. Finally, the pathway that we proposed to be implicated in these effects is PI3K-NOS-NO. Full article
Show Figures

Figure 1

Back to TopTop