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Pharmaceutics
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Proteins and Peptides as a Treatment for Cardiovascular Disease: From...
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Proteins and Peptides as a Treatment for Cardiovascular Disease: From Bacteria to Human

A special issue of Pharmaceutics (ISSN 1999-4923). This special issue belongs to the section "Biologics and Biosimilars".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 7944

Special Issue Editor

Dr. Guerrero-Beltrán Carlos Enrique

E-Mail Website
Guest Editor
Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Medicina Cardiovascular y Metabolómica, Monterrey 64710, Mexico
Interests: cardiovascular diseases; heat shock proteins; antioxidants; immunomodulation; vaccines; inflammation; nanotoxicology; oxidative stress; cell signaling, therapeutics; proteins; peptides; exosomes.

Special Issue Information

Dear Colleagues,

Cardiovascular diseases that conclude with the pathological hypertrophy of the heart continue to be an important factor contributing to the progression toward the final stage of heart failure, where current treatments and interventions are not effective enough to reduce mortality. Even though cell injury and pathological hypertrophy are the culmination of the constant activation and accumulation of different pathways and stress responses, pathogens or self-proteins and peptides seem to play an important role in triggering the initial steps of unwanted progression toward these maladaptive events with the ultimate production of pro-hypertrophy and pro-inflammatory markers.

Protein and peptide dysregulation is well documented in processes such as metabolic diseases, obesity, atherosclerosis, diabetes mellitus, heart failure or even other pathologies, like cancer. Nevertheless, the role of these molecules as major mediators of cell, and tissue injury/damage needs to be studied in depth. Pathogen proteins or autologous proteins/peptides can act as strong modulators, with beneficial therapeutic values for their potential use as candidate targets in heart, kidney or lung by autocrine-, paracrine-, endocrine-, and pathogen-induced diseases. This Special Issue aims to explore the uses of proteins and peptides in silico, in vitro, and in vivo as novel therapeutic tools in the development of potent cell modulators or immunomodulators to block pathogens or to enhance protection against self-dysregulated mechanisms related to the development of cardiovascular diseases. We invite you to submit original works, research papers, reviews, and short communications. 

Dr. Guerrero-Beltrán Enrique
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. Pharmaceutics is an international peer-reviewed open access monthly 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 2900 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 diseases
  • proteins and peptides
  • bioactive proteins and peptides
  • therapeutic proteins and peptides
  • pathogen and antimicrobial proteins
  • anti-inflammatory proteins
  • protein and peptide immunomodulation
  • in silico, in vitro, and in vivo protein approach

Published Papers (3 papers)

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Research

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19 pages, 8741 KiB  
Article
Computational Design and Biological Evaluation of Analogs of Lupin Peptide P5 Endowed with Dual PCSK9/HMG-CoAR Inhibiting Activity
by Carmen Lammi, Enrico M. A. Fassi, Jianqiang Li, Martina Bartolomei, Giulia Benigno, Gabriella Roda, Anna Arnoldi and Giovanni Grazioso
Pharmaceutics 2022, 14(3), 665; https://doi.org/10.3390/pharmaceutics14030665 - 18 Mar 2022
Cited by 12 | Viewed by 2280
Abstract
(1) Background: Proprotein convertase subtilisin/kexin 9 (PCSK9) is responsible for the degradation of the hepatic low-density lipoprotein receptor (LDLR), which regulates the circulating cholesterol level. In this field, we discovered natural peptides derived from lupin that showed PCSK9 inhibitory activity. Among these, the [...] Read more.
(1) Background: Proprotein convertase subtilisin/kexin 9 (PCSK9) is responsible for the degradation of the hepatic low-density lipoprotein receptor (LDLR), which regulates the circulating cholesterol level. In this field, we discovered natural peptides derived from lupin that showed PCSK9 inhibitory activity. Among these, the most active peptide, known as P5 (LILPHKSDAD), reduced the protein-protein interaction between PCSK9 and LDLR with an IC50 equals to 1.6 µM and showed a dual hypocholesterolemic activity, since it shows complementary inhibition of the 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoAR). (2) Methods: In this study, by a computational approach, the P5 primary structure was optimized to obtain new analogs with improved affinity to PCSK9. Then, biological assays were carried out for fully characterizing the dual cholesterol-lowering activity of the P5 analogs by using both biochemical and cellular techniques. (3) Results: A new peptide, P5-Best (LYLPKHSDRD) displayed improved PCSK9 (IC50 0.7 µM) and HMG-CoAR (IC50 88.9 µM) inhibitory activities. Moreover, in vitro biological assays on cells demonstrated that, not only P5-Best, but all tested peptides maintained the dual PCSK9/HMG-CoAR inhibitory activity and remarkably P5-Best exerted the strongest hypocholesterolemic effect. In fact, in the presence of this peptide, the ability of HepG2 cells to absorb extracellular LDL was improved by up to 254%. (4) Conclusions: the atomistic details of the P5-Best/PCSK9 and P5-Best/HMG-CoAR interactions represent a reliable starting point for the design of new promising molecular entities endowed with hypocholesterolemic activity. Full article
(This article belongs to the Special Issue Proteins and Peptides as a Treatment for Cardiovascular Disease: From Bacteria to Human)
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Review

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31 pages, 1924 KiB  
Review
APJ as Promising Therapeutic Target of Peptide Analogues in Myocardial Infarction- and Hypertension-Induced Heart Failure
by Daniela Rossin, Roberto Vanni, Marco Lo Iacono, Caterina Cristallini, Claudia Giachino and Raffaella Rastaldo
Pharmaceutics 2023, 15(5), 1408; https://doi.org/10.3390/pharmaceutics15051408 - 04 May 2023
Cited by 2 | Viewed by 1960
Abstract
The widely expressed G protein-coupled apelin receptor (APJ) is activated by two bioactive endogenous peptides, apelin and ELABELA (ELA). The apelin/ELA-APJ-related pathway has been found involved in the regulation of many physiological and pathological cardiovascular processes. Increasing studies are deepening the role of [...] Read more.
The widely expressed G protein-coupled apelin receptor (APJ) is activated by two bioactive endogenous peptides, apelin and ELABELA (ELA). The apelin/ELA-APJ-related pathway has been found involved in the regulation of many physiological and pathological cardiovascular processes. Increasing studies are deepening the role of the APJ pathway in limiting hypertension and myocardial ischaemia, thus reducing cardiac fibrosis and adverse tissue remodelling, outlining APJ regulation as a potential therapeutic target for heart failure prevention. However, the low plasma half-life of native apelin and ELABELA isoforms lowered their potential for pharmacological applications. In recent years, many research groups focused their attention on studying how APJ ligand modifications could affect receptor structure and dynamics as well as its downstream signalling. This review summarises the novel insights regarding the role of APJ-related pathways in myocardial infarction and hypertension. Furthermore, recent progress in designing synthetic compounds or analogues of APJ ligands able to fully activate the apelinergic pathway is reported. Determining how to exogenously regulate the APJ activation could help to outline a promising therapy for cardiac diseases. Full article
(This article belongs to the Special Issue Proteins and Peptides as a Treatment for Cardiovascular Disease: From Bacteria to Human)
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18 pages, 2176 KiB  
Review
Transthyretin Stabilizers and Seeding Inhibitors as Therapies for Amyloid Transthyretin Cardiomyopathy
by Paolo Morfino, Alberto Aimo, Giuseppe Vergaro, Chiara Sanguinetti, Vincenzo Castiglione, Maria Franzini, Marco Alfonso Perrone and Michele Emdin
Pharmaceutics 2023, 15(4), 1129; https://doi.org/10.3390/pharmaceutics15041129 - 03 Apr 2023
Cited by 3 | Viewed by 2071
Abstract
Transthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is a progressive and increasingly recognized cause of heart failure which is associated with high mortality and morbidity. ATTR-CM is characterized by the misfolding of TTR monomers and their deposition within the myocardium as amyloid fibrils. The standard [...] Read more.
Transthyretin (TTR) amyloid cardiomyopathy (ATTR-CM) is a progressive and increasingly recognized cause of heart failure which is associated with high mortality and morbidity. ATTR-CM is characterized by the misfolding of TTR monomers and their deposition within the myocardium as amyloid fibrils. The standard of care for ATTR-CM consists of TTR-stabilizing ligands, such as tafamidis, which aim at maintaining the native structure of TTR tetramers, thus preventing amyloid aggregation. However, their efficacy in advanced-staged disease and after long-term treatment is still a source of concern, suggesting the existence of other pathogenetic factors. Indeed, pre-formed fibrils present in the tissue can further accelerate amyloid aggregation in a self-propagating process known as “amyloid seeding”. The inhibition of amyloidogenesis through TTR stabilizers combined with anti-seeding peptides may represent a novel strategy with additional benefits over current therapies. Finally, the role of stabilizing ligands needs to be reassessed in view of the promising results derived from trials which have evaluated alternative strategies, such as TTR silencers and immunological amyloid disruptors. Full article
(This article belongs to the Special Issue Proteins and Peptides as a Treatment for Cardiovascular Disease: From Bacteria to Human)
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