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Novel Molecular Targets in Cardiovascular Diseases 2.0
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Novel Molecular Targets in Cardiovascular Diseases 2.0

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

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 10118

Special Issue Editors

Dr. Erica Rurali

E-Mail Website
Guest Editor
Centro Cardiologico Monzino-IRCCS, Milan, Italy
Interests: cardiovascular sciences; rare diseases; vascular dysfunction; aortic aneurysm; diabetes; regenerative medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Alice Bonomi

E-Mail Website
Guest Editor
Centro Cardiologico Monzino, IRCCS, Via Parea, 4, 20138 Milan, Italy
Interests: cardiovascular biomarkers; cardiovascular risk calculator; biostatistics; diabetes; cardiovascular disease; epidemiology; prevention
Dr. Maria Cristina Vinci

E-Mail Website
Guest Editor
Unit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino—IRCCS, Milan, Italy
Interests: cellular pharmacology; stem/progenitor cell and vascular biology; epigenetics; diabetes; cardiovascular disease; regenerative medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are the leading causes of death and disability worldwide. Moreover, they represent an enormous burden for the healthcare systems of all countries. Despite any steps forward that have been achieved thanks to scientific and clinical research, it has been a while since novel drugs for cardiovascular diseases have been introduced into the clinical arena. Thus, the discovery of novel targets that can be exploited to develop new effective therapies is an impellent need to improve patient outcomes and limit healthcare expenses.

This Special Issue on “Novel Molecular Targets in Cardiovascular Diseases” will cover a selection of the most recent scientific studies and current review articles in the field of clinical, translational, and basic research dedicated to the discovery of biomarkers, molecular, and/or cellular mechanisms to be exploited as therapeutic targets or diagnostic tools to improve the outcome of patients with cardiovascular disease. Experimental papers, up-to-date review articles, and commentaries are all welcome.

Dr. Erica Rurali
Dr. Alice Bonomi
Dr. Maria Cristina Vinci
Guest Editors

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

  • biomarkers (diagnostic, prognostic and predictive)
  • novel molecular target
  • cardiac disease
  • vascular disease
  • translational research
  • new therapies

Related Special Issue

Published Papers (6 papers)

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Research

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19 pages, 7171 KiB  
Article
Nile Tilapia (Oreochromis niloticus) Patched1 Mutations Disrupt Cardiovascular Development and Vascular Integrity through Smoothened Signaling
by Xiang Liu, Changle Zhao, Lei Liu, Xi Peng, Jianeng Li, Wenjing Tao, Deshou Wang and Jing Wei
Int. J. Mol. Sci. 2024, 25(6), 3321; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25063321 - 15 Mar 2024
Viewed by 620
Abstract
Hedgehog (Hh) signaling is crucial in cardiovascular development and maintenance. However, the biological role of Patched1 (Ptch1), an inhibitory receptor of the Hh signaling pathway, remains elusive. In this study, a Ptch1 ortholog was characterized in Nile tilapia (Oreochromis niloticus), and [...] Read more.
Hedgehog (Hh) signaling is crucial in cardiovascular development and maintenance. However, the biological role of Patched1 (Ptch1), an inhibitory receptor of the Hh signaling pathway, remains elusive. In this study, a Ptch1 ortholog was characterized in Nile tilapia (Oreochromis niloticus), and its function was investigated through CRISPR/Cas9 gene knockout. When one-cell embryos were injected with CRISPR/Cas9 targeting ptch1, the mutation efficiency exceeded 70%. During 0–3 days post fertilization (dpf), no significant differences were observed between the ptch1 mutant group and the control group; at 4 dpf (0 day after hatching), about 10% of the larvae showed an angiogenesis defect and absence of blood flow; from 5 dpf, most larvae exhibited an elongated heart, large pericardial cavity, and blood leakage and coagulation, ultimately dying during the 6–8 dpf period due to the lack of blood circulation. Consistently, multiple differentially expressed genes related to angiogenesis, blood coagulation, and heart development were enriched in the ptch1 mutants. Furthermore, Smoothened (Smo) antagonist (cyclopamine) treatment of the ptch1 mutants greatly rescued the cardiovascular disorders. Collectively, our study suggests that Ptch1 is required for cardiovascular development and vascular integrity via Smo signaling, and excessive Hh signaling is detrimental to cardiovascular development. Full article
(This article belongs to the Special Issue Novel Molecular Targets in Cardiovascular Diseases 2.0)
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13 pages, 3991 KiB  
Article
SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation
by Min Liang, Zhaohua Cai, Yangjing Jiang, Huanhuan Huo, Linghong Shen and Ben He
Int. J. Mol. Sci. 2022, 23(20), 12637; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012637 - 20 Oct 2022
Cited by 7 | Viewed by 1648
Abstract
Myocardin is a master regulator of smooth muscle cell (SMC) differentiation, which induces the expression of smooth-muscle-specific genes through its direct association with serum response factor (SRF). During the past two decades, significant insights have been obtained regarding the regulatory control of myocardin [...] Read more.
Myocardin is a master regulator of smooth muscle cell (SMC) differentiation, which induces the expression of smooth-muscle-specific genes through its direct association with serum response factor (SRF). During the past two decades, significant insights have been obtained regarding the regulatory control of myocardin expression and transcriptional activity at the transcriptional, post-transcriptional, and post-translational levels. However, whether and how SUMOylation plays important roles in modulating myocardin function remain elusive. In this study, we found that myocardin is modified by SUMO-1 at lysine 573, which can be reversibly de-conjugated by SENP2. SUMO-1 modification promotes myocardin protein stability, whereas SENP2 facilitates its proteasome-dependent degradation. Moreover, we found that PIAS4 is the SUMO E3 ligase that enhances the SUMOylation and protein stability of myocardin. Most importantly, we found that SENP2 promotes phenotypic switching of VSMC. We therefore concluded that SENP2 promotes VSMC phenotypic switching via de-SUMOylation of myocardin and regulation of its protein stability. Full article
(This article belongs to the Special Issue Novel Molecular Targets in Cardiovascular Diseases 2.0)
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19 pages, 2667 KiB  
Article
Neurotoxic Effect of Doxorubicin Treatment on Cardiac Sympathetic Neurons
by Nicola Moro, Lolita Dokshokova, Induja Perumal Vanaja, Valentina Prando, Sophie Julie A Cnudde, Anna Di Bona, Riccardo Bariani, Leonardo Schirone, Barbara Bauce, Annalisa Angelini, Sebastiano Sciarretta, Alessandra Ghigo, Marco Mongillo and Tania Zaglia
Int. J. Mol. Sci. 2022, 23(19), 11098; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911098 - 21 Sep 2022
Cited by 7 | Viewed by 2207
Abstract
Doxorubicin (DOXO) remains amongst the most commonly used anti-cancer agents for the treatment of solid tumors, lymphomas, and leukemias. However, its clinical use is hampered by cardiotoxicity, characterized by heart failure and arrhythmias, which may require chemotherapy interruption, with devastating consequences on patient [...] Read more.
Doxorubicin (DOXO) remains amongst the most commonly used anti-cancer agents for the treatment of solid tumors, lymphomas, and leukemias. However, its clinical use is hampered by cardiotoxicity, characterized by heart failure and arrhythmias, which may require chemotherapy interruption, with devastating consequences on patient survival and quality of life. Although the adverse cardiac effects of DOXO are consolidated, the underlying mechanisms are still incompletely understood. It was previously shown that DOXO leads to proteotoxic cardiomyocyte (CM) death and myocardial fibrosis, both mechanisms leading to mechanical and electrical dysfunction. While several works focused on CMs as the culprits of DOXO-induced arrhythmias and heart failure, recent studies suggest that DOXO may also affect cardiac sympathetic neurons (cSNs), which would thus represent additional cells targeted in DOXO-cardiotoxicity. Confocal immunofluorescence and morphometric analyses revealed alterations in SN innervation density and topology in hearts from DOXO-treated mice, which was consistent with the reduced cardiotropic effect of adrenergic neurons in vivo. Ex vivo analyses suggested that DOXO-induced denervation may be linked to reduced neurotrophic input, which we have shown to rely on nerve growth factor, released from innervated CMs. Notably, similar alterations were observed in explanted hearts from DOXO-treated patients. Our data demonstrate that chemotherapy cardiotoxicity includes alterations in cardiac innervation, unveiling a previously unrecognized effect of DOXO on cardiac autonomic regulation, which is involved in both cardiac physiology and pathology, including heart failure and arrhythmias. Full article
(This article belongs to the Special Issue Novel Molecular Targets in Cardiovascular Diseases 2.0)
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13 pages, 1544 KiB  
Article
The Ambivalence of Connexin43 Gap Peptides in Cardioprotection of the Isolated Heart against Ischemic Injury
by Aleksander Tank Falck, Bjarte Aarmo Lund, David Johansen, Trine Lund and Kirsti Ytrehus
Int. J. Mol. Sci. 2022, 23(17), 10197; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231710197 - 05 Sep 2022
Cited by 1 | Viewed by 1615
Abstract
The present study investigates infarct-reducing effects of blocking ischemia-induced opening of connexin43 hemichannels using peptides Gap19, Gap26 or Gap27. Cardioprotection by ischemic preconditioning (IPC) and Gap peptides was compared, and combined treatment was tested in isolated, perfused male rat hearts using function and [...] Read more.
The present study investigates infarct-reducing effects of blocking ischemia-induced opening of connexin43 hemichannels using peptides Gap19, Gap26 or Gap27. Cardioprotection by ischemic preconditioning (IPC) and Gap peptides was compared, and combined treatment was tested in isolated, perfused male rat hearts using function and infarct size after global ischemia, high-resolution respirometry of isolated mitochondrial and peptide binding kinetics as endpoints. The Gap peptides reduced infarct size significantly when given prior to ischemia plus at reperfusion (Gap19 76.2 ± 2.7, Gap26 72.9 ± 5.8 and Gap27 71.9 ± 5.8% of untreated control infarcts, mean ± SEM). Cardioprotection was lost when Gap26, but not Gap27 or Gap19, was combined with triggering IPC (IPC 73.4 ± 5.5, Gap19-IPC 60.9 ± 5.1, Gap26-IPC 109.6 ± 7.8, Gap27-IPC 56.3 ± 8.0% of untreated control infarct). Binding stability of peptide Gap26 to its specific extracellular loop sequence (EL2) of connexin43 was stronger than Gap27 to its corresponding loop EL1 (dissociation rate constant Kd 0.061 ± 0.004 vs. 0.0043 ± 0.0001 s−1, mean ± SD). Mitochondria from IPC hearts showed slightly but significantly reduced respiratory control ratio (RCR). In vitro addition of Gap peptides did not significantly alter respiration. If transient hemichannel activity is part of the IPC triggering event, inhibition of IPC triggering stimuli might limit the use of cardioprotective Gap peptides. Full article
(This article belongs to the Special Issue Novel Molecular Targets in Cardiovascular Diseases 2.0)
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Review

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12 pages, 1195 KiB  
Review
Proenkephalin as a Novel Prognostic Marker in Heart Failure Patients: A Systematic Review and Meta-Analysis
by Noppachai Siranart, Khamik Laohasurayotin, Tanattida Phanthong, Walit Sowalertrat, Aekarach Ariyachaipanich and Ronpichai Chokesuwattanaskul
Int. J. Mol. Sci. 2023, 24(5), 4887; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054887 - 03 Mar 2023
Cited by 2 | Viewed by 1572
Abstract
Over the last several years, the use of biomarkers in the diagnosis of patients with heart failure (HF) has skyrocketed. Natriuretic peptides are currently the most widely used biomarker in the diagnosis and prognosis of individuals with HF. Proenkephalin (PENK) activates delta-opioid receptors [...] Read more.
Over the last several years, the use of biomarkers in the diagnosis of patients with heart failure (HF) has skyrocketed. Natriuretic peptides are currently the most widely used biomarker in the diagnosis and prognosis of individuals with HF. Proenkephalin (PENK) activates delta-opioid receptors in cardiac tissue, resulting in a decreased myocardial contractility and heart rate. However, the goal of this meta-analysis is to evaluate the association between the PENK level at the time of admission and prognosis in patients with HF, such as all-cause mortality, rehospitalization, and decreasing renal function. High PENK levels have been associated with a worsened prognosis in patients with HF. Full article
(This article belongs to the Special Issue Novel Molecular Targets in Cardiovascular Diseases 2.0)
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25 pages, 866 KiB  
Review
The Role of Neutrophils in Lower Limb Peripheral Artery Disease: State of the Art and Future Perspectives
by Giacomo Buso, Elisabetta Faggin, Nathalie Rosenblatt-Velin, Maxime Pellegrin, Silvia Galliazzo, Luca Calanca, Marcello Rattazzi and Lucia Mazzolai
Int. J. Mol. Sci. 2023, 24(2), 1169; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24021169 - 06 Jan 2023
Cited by 3 | Viewed by 1731
Abstract
In recent years, increasing attention has been paid to the role of neutrophils in cardiovascular (CV) disease (CVD) with evidence supporting their role in the initiation, progression, and rupture of atherosclerotic plaque. Although these cells have long been considered as terminally differentiated cells [...] Read more.
In recent years, increasing attention has been paid to the role of neutrophils in cardiovascular (CV) disease (CVD) with evidence supporting their role in the initiation, progression, and rupture of atherosclerotic plaque. Although these cells have long been considered as terminally differentiated cells with a relatively limited spectrum of action, recent research has revealed intriguing novel cellular functions, including neutrophil extracellular trap (NET) generation and inflammasome activation, which have been linked to several human diseases, including CVD. While most research to date has focused on the role of neutrophils in coronary artery and cerebrovascular diseases, much less information is available on lower limb peripheral artery disease (PAD). PAD is a widespread condition associated with great morbidity and mortality, though physician and patient awareness of the disease remains low. To date, several studies have produced some evidence on the role of certain biomarkers of neutrophil activation in this clinical setting. However, the etiopathogenetic role of neutrophils, and in particular of some of the newly discovered mechanisms, has yet to be fully elucidated. In the future, complementary assessment of neutrophil activity should improve CV risk stratification and provide personalized treatments to patients with PAD. This review aims to summarize the basic principles and recent advances in the understanding of neutrophil biology, current knowledge about the role of neutrophils in atherosclerosis, as well as available evidence on their role of PAD. Full article
(This article belongs to the Special Issue Novel Molecular Targets in Cardiovascular Diseases 2.0)
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