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Biomedicines
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Angiogenesis
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Angiogenesis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 12057

Special Issue Editors

Dr. Angela Orecchia

E-Mail Website
Guest Editor
Laboratory of Molecular and Cell Biology, IDI-IRCCS, Rome, Italy
Interests: cellular biology; cellular signaling; endothelial cell behavior
Dr. Cristina M. Failla

E-Mail Website
Guest Editor
Experimental Immunology Laboratory, IDI-IRCCS, Rome, Italy
Interests: endothelial cells in inflammatory processes and in cell-to-cell cross talks; immune responses to skin tumors; 3D alternative models of human skin
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The aim of this Special Issue is to collect publications that focus on to the angiogenesis key processes which influence human health.

Angiogenesis is the growth of blood vessels from the existing vasculature: metabolically active tissue is no more than a few hundred micrometers from a blood capillary, which is formed through the process of angiogenesis.

Angiogenesis occurs throughout life in both healthy subjects and subjects suffering from a disease; therefore, the control of angiogenesis has a therapeutic value and has been a field of significant interest during the past 40 years research.

Stimulation of angiogenesis can be therapeutic in ischemic heart disease, peripheral arterial disease, and wound healing. Inhibiting angiogenesis can be therapeutic in cancer, ophthalmic conditions, rheumatoid arthritis, and other pathological conditions.

One group of essential growth factor receptors in angiogenesis are vascular endothelial growth factor receptors (VEGFRs), a subfamily of receptor tyrosine kinases (RTKs). Multiple VEGF ligands with different preference and capability bind to VEGFRs and activate them in homo- and heterodimeric manners, representing a challenge for the study of their selective biochemical and cellular signaling in endothelial cell backgrounds and the role in leading angiogenesis processes.

This Special Issue welcomes original articles and reviews focused on the novelties in the angiogenesis field both in human health and disease.

Dr. Angela Orecchia
Dr. Cristina M. Failla
Guest Editors

Manuscript Submission Information

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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. Biomedicines 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 2600 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

  • Vascular Endothelial Growth Factor Receptor-1 (VEGFR-1)
  • Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2)
  • angiogenesis
  • vasculogenesis
  • receptor tyrosine kinases
  • tumor angiogenesis
  • angiogenesis in health and disease

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Published Papers (7 papers)

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Research

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17 pages, 6313 KiB  
Article
Could CH3-M6P Be a Potential Dual-Functioning Candidate for Bone Regeneration?
by Fidan Huseynova, Cătălina Ionescu, Frederic Cuisinier, Irada Huseynova, Alamdar Mammadov and Véronique Barragan-Montero
Biomedicines 2024, 12(12), 2697; https://doi.org/10.3390/biomedicines12122697 - 26 Nov 2024
Viewed by 372
Abstract
Background: CI-RM6P has different binding sites with affinities for both M6P and IGF2, plays a role in the regulation of the TGF-β and IGF pathways that is important for controlling cell growth and differentiation. We hypothesize that previously synthesised derivative of M6P [...] Read more.
Background: CI-RM6P has different binding sites with affinities for both M6P and IGF2, plays a role in the regulation of the TGF-β and IGF pathways that is important for controlling cell growth and differentiation. We hypothesize that previously synthesised derivative of M6P could be an alternative candidate for bone tissue regeneration in terms of higher binding affinity, stability in human serum, low cost and temporal delivery. Methods: CH3-M6P is synthesised based on previously described protocol; mesenchymal origin of isolated DPSCs was assessed by flow cytometry and AR staining prior to alkaline phosphatase (ALP) activity test, qPCR to evaluate differentiation specific marker expression, immunofluoresence, and SEM/EDS to evaluate organic and inorganic matrix formation; and rat aortic ring model to evaluate angiogenic effect of molecule. Results: CH3-M6P upregulated ALP activity, the expression of the ALP, Col1, RunX2, Mef2C, TGFβ1, TGFβ1R, TGFβ2, and Smad3 genes under osteogenic conditions. The results of immunofluorescence and SEM/EDS studies did not show enhancing effect on matrix formation. As we observed, the induction effect of CH3-M6P on the expression of angiogenic genes such as SMAD3 and TGFβ1R, even under osteogenic conditions, within the scope of research, we checked the angiogenic effect of the molecule and compared it to VEGF, showing that the CH3-M6P is really angiogenic. Conclusions: Our findings provide an important clue for the further exploration of the molecule, which can be necessary to enhance the capability of the commonly used osteomedium, possibly leading to the development of bone-forming drugs and has the potential to be a dual-functioning molecule for bone tissue engineering. Full article
(This article belongs to the Special Issue Angiogenesis)
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25 pages, 8174 KiB  
Article
Unraveling the Complex Molecular Interplay and Vascular Adaptive Changes in Hypertension-Induced Kidney Disease
by Lyubomir Gaydarski, Iva N. Dimitrova, Stancho Stanchev, Alexandar Iliev, Georgi Kotov, Vidin Kirkov, Nikola Stamenov, Tihomir Dikov, Georgi P. Georgiev and Boycho Landzhov
Biomedicines 2024, 12(8), 1723; https://doi.org/10.3390/biomedicines12081723 - 1 Aug 2024
Viewed by 819
Abstract
Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate [...] Read more.
Angiogenesis, the natural mechanism by which fresh blood vessels develop from preexisting ones, is altered in arterial hypertension (AH), impacting renal function. Studies have shown that hypertension-induced renal damage involves changes in capillary density (CD), indicating alterations in vascularization. We aimed to elucidate the role of the apelin receptor (APLNR), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF) in hypertension-induced renal damage. We used two groups of spontaneously hypertensive rats aged 6 and 12 months, representing different stages of AH, and compared them to age-matched normotensive controls. The kidney tissue samples were prepared through a well-established protocol. All data analysis was conducted with a dedicated software program. APLNR was localized in tubular epithelial cells and the endothelial cells of the glomeruli, with higher expression in older SHRs. The localization of nNOS and VEGF was similar. The expression of APLNR and nNOS increased with AH progression, while VEGF levels decreased. CD was lower in young SHRs compared to controls and decreased significantly in older SHRs in comparison to age-matched controls. Our statistical analysis revealed significant differences in molecule expression between age groups and varying correlations between the expression of the three molecules and CD. Full article
(This article belongs to the Special Issue Angiogenesis)
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16 pages, 3490 KiB  
Article
Computational Insights into the Interplay of Mechanical Forces in Angiogenesis
by Ana Guerra, Jorge Belinha, Christiane Salgado, Fernando Jorge Monteiro and Renato Natal Jorge
Biomedicines 2024, 12(5), 1045; https://doi.org/10.3390/biomedicines12051045 - 9 May 2024
Viewed by 939
Abstract
This study employs a meshless computational model to investigate the impacts of compression and traction on angiogenesis, exploring their effects on vascular endothelial growth factor (VEGF) diffusion and subsequent capillary network formation. Three distinct initial domain geometries were defined to simulate variations in [...] Read more.
This study employs a meshless computational model to investigate the impacts of compression and traction on angiogenesis, exploring their effects on vascular endothelial growth factor (VEGF) diffusion and subsequent capillary network formation. Three distinct initial domain geometries were defined to simulate variations in endothelial cell sprouting and VEGF release. Compression and traction were applied, and the ensuing effects on VEGF diffusion coefficients were analysed. Compression promoted angiogenesis, increasing capillary network density. The reduction in the VEGF diffusion coefficient under compression altered VEGF concentration, impacting endothelial cell migration patterns. The findings were consistent across diverse simulation scenarios, demonstrating the robust influence of compression on angiogenesis. This computational study enhances our understanding of the intricate interplay between mechanical forces and angiogenesis. Compression emerges as an effective mediator of angiogenesis, influencing VEGF diffusion and vascular pattern. These insights may contribute to innovative therapeutic strategies for angiogenesis-related disorders, fostering tissue regeneration and addressing diseases where angiogenesis is crucial. Full article
(This article belongs to the Special Issue Angiogenesis)
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Review

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23 pages, 3087 KiB  
Review
Animal Models of Retinopathy of Prematurity: Advances and Metabolic Regulators
by Meenakshi Maurya, Chi-Hsiu Liu, Kiran Bora, Neetu Kushwah, Madeline C. Pavlovich, Zhongxiao Wang and Jing Chen
Biomedicines 2024, 12(9), 1937; https://doi.org/10.3390/biomedicines12091937 - 23 Aug 2024
Viewed by 887
Abstract
Retinopathy of prematurity (ROP) is a primary cause of visual impairment and blindness in premature newborns, characterized by vascular abnormalities in the developing retina, with microvascular alteration, neovascularization, and in the most severe cases retinal detachment. To elucidate the pathophysiology and develop therapeutics [...] Read more.
Retinopathy of prematurity (ROP) is a primary cause of visual impairment and blindness in premature newborns, characterized by vascular abnormalities in the developing retina, with microvascular alteration, neovascularization, and in the most severe cases retinal detachment. To elucidate the pathophysiology and develop therapeutics for ROP, several pre-clinical experimental models of ROP were developed in different species. Among them, the oxygen-induced retinopathy (OIR) mouse model has gained the most popularity and critically contributed to our current understanding of pathological retinal angiogenesis and the discovery of potential anti-angiogenic therapies. A deeper comprehension of molecular regulators of OIR such as hypoxia-inducible growth factors including vascular endothelial growth factors as primary perpetrators and other new metabolic modulators such as lipids and amino acids influencing pathological retinal angiogenesis is also emerging, indicating possible targets for treatment strategies. This review delves into the historical progressions that gave rise to the modern OIR models with a focus on the mouse model. It also reviews the fundamental principles of OIR, recent advances in its automated assessment, and a selected summary of metabolic investigation enabled by OIR models including amino acid transport and metabolism. Full article
(This article belongs to the Special Issue Angiogenesis)
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20 pages, 951 KiB  
Review
Recent Insights into Cellular and Molecular Mechanisms of Defective Angiogenesis in Systemic Sclerosis
by Eloisa Romano, Irene Rosa, Bianca Saveria Fioretto and Mirko Manetti
Biomedicines 2024, 12(6), 1331; https://doi.org/10.3390/biomedicines12061331 - 14 Jun 2024
Viewed by 1210
Abstract
In systemic sclerosis (SSc, or scleroderma), defective angiogenesis, clinically manifesting with abnormal capillary architecture and severe capillary reduction, represents a hallmark of early-stage disease, usually preceding the onset of tissue fibrosis, and is caused by several cellular and molecular mechanisms affecting microvascular endothelial [...] Read more.
In systemic sclerosis (SSc, or scleroderma), defective angiogenesis, clinically manifesting with abnormal capillary architecture and severe capillary reduction, represents a hallmark of early-stage disease, usually preceding the onset of tissue fibrosis, and is caused by several cellular and molecular mechanisms affecting microvascular endothelial cells with different outcomes. Indeed, once damaged, endothelial cells can be dysfunctionally activated, thus becoming unable to undergo angiogenesis and promoting perivascular inflammation. They can also undergo apoptosis, transdifferentiate into profibrotic myofibroblasts, or acquire a senescence-associated secretory phenotype characterized by the release of exosomes and several profibrotic and proinflammatory mediators. In this narrative review, we aimed to give a comprehensive overview of recent studies dealing with the cellular and molecular mechanisms underlying SSc defective angiogenesis and the related endothelial cell dysfunctions, mainly the endothelial-to-mesenchymal transition process. We also discussed potential novel vascular treatment strategies able to restore the angiogenic process and reduce the endothelial-to-mesenchymal transition in this complex disease. Full article
(This article belongs to the Special Issue Angiogenesis)
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15 pages, 1167 KiB  
Review
Vascular Endothelial Growth Factor (VEGF) and Its Role in the Cardiovascular System
by Kamila Florek, Dominik Mendyka and Krzysztof Gomułka
Biomedicines 2024, 12(5), 1055; https://doi.org/10.3390/biomedicines12051055 - 10 May 2024
Cited by 5 | Viewed by 3973
Abstract
Cardiovascular diseases remain the leading cause of death worldwide, with ischemic heart disease (IHD) as the most common. Ischemia-induced angiogenesis is a process in which vascular endothelial growth factor (VEGF) plays a crucial role. To conduct research in the field of VEGF’s association [...] Read more.
Cardiovascular diseases remain the leading cause of death worldwide, with ischemic heart disease (IHD) as the most common. Ischemia-induced angiogenesis is a process in which vascular endothelial growth factor (VEGF) plays a crucial role. To conduct research in the field of VEGF’s association in cardiovascular diseases, it is vital to understand its role in the physiological and pathological processes in the heart. VEGF-based therapies have demonstrated a promising role in preclinical studies. However, their potential in human therapies is currently under discussion. Furthermore, VEGF is considered a potential biomarker for collateral circulation assessment and heart failure (HF) mortality. Additionally, as VEGF is involved in angiogenesis, there is a need to elucidate the impact of VEGF-targeted therapies in terms of cardiovascular side effects. Full article
(This article belongs to the Special Issue Angiogenesis)
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21 pages, 2649 KiB  
Review
Decoding Tumor Angiogenesis for Therapeutic Advancements: Mechanistic Insights
by Geetika Kaur and Bipradas Roy
Biomedicines 2024, 12(4), 827; https://doi.org/10.3390/biomedicines12040827 - 9 Apr 2024
Cited by 1 | Viewed by 2539
Abstract
Tumor angiogenesis, the formation of new blood vessels within the tumor microenvironment, is considered a hallmark of cancer progression and represents a crucial target for therapeutic intervention. The tumor microenvironment is characterized by a complex interplay between proangiogenic and antiangiogenic factors, regulating the [...] Read more.
Tumor angiogenesis, the formation of new blood vessels within the tumor microenvironment, is considered a hallmark of cancer progression and represents a crucial target for therapeutic intervention. The tumor microenvironment is characterized by a complex interplay between proangiogenic and antiangiogenic factors, regulating the vascularization necessary for tumor growth and metastasis. The study of angiogenesis involves a spectrum of techniques, spanning from biomarker assessment to advanced imaging modalities. This comprehensive review aims to provide insights into the molecular intricacies, regulatory dynamics, and clinical implications of tumor angiogenesis. By delving into these aspects, we gain a deeper understanding of the processes driving vascularization in tumors, paving the way for the development of novel and effective antiangiogenic therapies in the fight against cancer. Full article
(This article belongs to the Special Issue Angiogenesis)
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