Angiogenesis in Health and Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 7813

Special Issue Editor


E-Mail Website
Guest Editor
1. Department of Pediatrics, Medical College of Wisconsin, Suite C410, Children Corporate Center, 999N 92nd Street, Milwaukee, WI 53226, USA
2. Children’s Research Institute, Medical College of Wisconsin, 8701 W Watertown Plank Rd., Wauwatosa, WI 53226, USA
Interests: neonatal-perinatal medicine; prematurity; neonatal disorders; free radicals research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Angiogenesis plays a critical role in fetal development, postnatal growth, recovery from injury, cancer progression and metastasis, inflammation, and metabolic disorders. In some situations, both coordinated angiogenesis and aberrant angiogenesis can co-exist in the same organ. Understanding how coordinated angiogenesis is achieved and the mechanisms by which aberrant angiogenesis occurs in different biologic contexts can help us gain a better idea of how to assist healthy organ growth and modulate disease progression. In this Special Issue, we will focus on the metabolisms that affect angiogenesis, genetic and epigenetic modulations of angiogenesis, and innovative methods that can either assist coordinated angiogenesis or inhibit unwanted aberrant angiogenesis. Review articles or research studies relating to healthy or deranged angiogenesis are welcome.

Dr. Ru-Jeng Teng
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. 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

  • angiogenesis
  • angiogenic factors
  • endothelial cells
  • smooth muscle cells
  • reactive oxygen species
  • nitric oxide
  • oxidative phosphorylation
  • glycolysis
  • transcription factor
  • Notch signaling
  • mitochondria
  • endoplasmic reticulum
  • development
  • disease
  • cancer

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 (3 papers)

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

Research

21 pages, 3657 KiB  
Article
Scandium-44 Radiolabeled Peptide and Peptidomimetic Conjugates Targeting Neuropilin-1 Co-Receptor as Potential Tools for Cancer Diagnosis and Anti-Angiogenic Therapy
by Katarzyna Masłowska, Patrycja Redkiewicz, Paweł Krzysztof Halik, Ewa Witkowska, Dagmara Tymecka, Rafał Walczak, Jarosław Choiński, Aleksandra Misicka and Ewa Gniazdowska
Biomedicines 2023, 11(2), 564; https://doi.org/10.3390/biomedicines11020564 - 15 Feb 2023
Cited by 4 | Viewed by 2029
Abstract
Pathological angiogenesis, resulting from an imbalance between anti- and pro-angiogenic factors, plays a pivotal role in tumor growth, development and metastasis. The inhibition of the angiogenesis process by the VEGF/VEGFR-2/NRP-1 pathway raises interest in the search for such interaction inhibitors for the purpose [...] Read more.
Pathological angiogenesis, resulting from an imbalance between anti- and pro-angiogenic factors, plays a pivotal role in tumor growth, development and metastasis. The inhibition of the angiogenesis process by the VEGF/VEGFR-2/NRP-1 pathway raises interest in the search for such interaction inhibitors for the purpose of the early diagnosis and treatment of angiogenesis-dependent diseases. In this work we designed and tested peptide-based radiocompounds that selectively bind to the neuropilin-1 co-receptor and prevent the formation of the pro-angiogenic VEGF-A165/NRP-1 complex. Three biomolecules, A7R and retro-inverso DR7A peptides, and the branched peptidomimetic Lys(hArg)-Dab-Pro-Arg (K4R), conjugated with macrocyclic chelator through two linkers’ types, were labeled with theranostic scandium-44 radionuclide, and studied in vitro as potential targeted radiopharmaceuticals. ELISA (enzyme-linked immunosorbent assay) studies showed no negative effect of the introduced biomolecules’ changes and high NRP-1 affinity in the case of A7R- and K4R-radiocompounds and a lack affinity for DR7A-radiocompounds. All radiopeptides showed a hydrophilic nature as well as high stability against ligand exchange reactions in cysteine/histidine solutions. Unfortunately, all radiocompounds showed unsatisfactory nano-scale stability in human serum, especially for use as therapeutic radioagents. Further work is ongoing and focused on the search for angiogenesis inhibitors that are more human serum stable. Full article
(This article belongs to the Special Issue Angiogenesis in Health and Disease)
Show Figures

Graphical abstract

11 pages, 1264 KiB  
Article
TGFβ1 Induces Senescence and Attenuated VEGF Production in Retinal Pericytes
by Dragana Avramovic, Sébastien A. Archaimbault, Alicia M. Kemble, Sabine Gruener, Mirjana Lazendic and Peter D. Westenskow
Biomedicines 2022, 10(6), 1404; https://doi.org/10.3390/biomedicines10061404 - 14 Jun 2022
Cited by 3 | Viewed by 2751
Abstract
Diabetic retinopathy (DR) is a microvascular disease of the retina and a serious complication of type I and type II diabetes mellitus. DR affects working-age populations and can cause permanent vision loss if left untreated. The standard of care for proliferative DR is [...] Read more.
Diabetic retinopathy (DR) is a microvascular disease of the retina and a serious complication of type I and type II diabetes mellitus. DR affects working-age populations and can cause permanent vision loss if left untreated. The standard of care for proliferative DR is inhibiting VEGF. However, the mechanisms that induce excessive VEGF production in the retina remain elusive, although some evidence links elevated VEGF in the diabetic retina with local and systemic TGFβ1 upexpression. Here, we present evidence from animal models of disease suggesting that excessive TGFβ1 production in the early DR is correlated with VEGF mRNA and protein production by senescent pericytes and other retinal cells. Collectively, these results confirm that TGFβ1 is strongly implicated in the vascular complications of DR. Full article
(This article belongs to the Special Issue Angiogenesis in Health and Disease)
Show Figures

Figure 1

20 pages, 5614 KiB  
Article
Identification of Novel Vascular Genes Downstream of Islet2 and Nr2f1b Transcription Factors
by Ru-Fang Li, Yi-Shan Wang, Fu-I Lu, Yi-Shan Huang, Chien-Chih Chiu, Ming-Hong Tai and Chang-Yi Wu
Biomedicines 2022, 10(6), 1261; https://doi.org/10.3390/biomedicines10061261 - 27 May 2022
Cited by 3 | Viewed by 2163
Abstract
The genetic regulation of vascular development is not elucidated completely. We previously characterized the transcription factors Islet2 (Isl2) and Nr2f1b as being critical for vascular growth. In this study, we further performed combinatorial microarrays to identify genes that are potentially regulated by these [...] Read more.
The genetic regulation of vascular development is not elucidated completely. We previously characterized the transcription factors Islet2 (Isl2) and Nr2f1b as being critical for vascular growth. In this study, we further performed combinatorial microarrays to identify genes that are potentially regulated by these factors. We verified the changed expression of several targets in isl2/nr2f1b morphants. Those genes expressed in vessels during embryogenesis suggested their functions in vascular development. We selectively assayed a potential target follistatin a (fsta). Follistatin is known to inhibit BMP, and BMP signaling has been shown to be important for angiogenesis. However, the fsta’s role in vascular development has not been well studied. Here, we showed the vascular defects in ISV growth and CVP patterning while overexpressing fsta in the embryo, which mimics the phenotype of isl2/nr2f1b morphants. The vascular abnormalities are likely caused by defects in migration and proliferation. We further observed the altered expression of vessel markers consistent with the vascular defects in (fli:fsta) embryos. We showed that the knockdown of fsta can rescue the vascular defects in (fli:fsta) fish, suggesting the functional specificity of fsta. Moreover, the decreased expression of fsta rescues abnormal vessel growth in isl2 and nr2f1b morphants, indicating that fsta functions downstream of isl2/nr2f1b. Lastly, we showed that Isl2/Nr2f1b control vascular development, via Fsta–BMP signaling in part. Collectively, our microarray data identify many interesting genes regulated by isl2/nr2f1b, which likely function in the vasculature. Our research provides useful information on the genetic control of vascular development. Full article
(This article belongs to the Special Issue Angiogenesis in Health and Disease)
Show Figures

Figure 1

Back to TopTop