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Angiogenesis in Disease 2.0

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: closed (30 June 2023) | Viewed by 5436

Special Issue Editors


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Guest Editor
Department of Pharmacy, University of Pisa, 56126 Pisa, Italy
Interests: bioinorganic chemistry; coordination chemistry; neurochemistry; angiogenesis; metal ions; peptides
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, 56126 Pisa, Italy
Interests: neurochemistry; neurodegeneration; signaling: receptors interactions; receptor metabolism; life/death/differentiation signaling; traslocator protein

E-Mail Website
Guest Editor
Department of Pharmacy, University of Pisa, 56126 Pisa, Italy
Interests: cell signaling; signal transduction; cell proliferation; apoptosis; cell line culture; primary cell culture; immunoprecipitation; cancer biology

Special Issue Information

Dear Colleagues,

Angiogenesis is the physiological process by which new blood capillaries form from the existing vasculature.

Excessive angiogenesis has been implicated, directly or indirectly, in many disorders and among them cancer, autoimmune diseases, diabetic retinopathy, rheumatoid arthritis and atherosclerosis. Conversely, insufficient vascularization and inadequate blood vessel growth can underpin or contribute to cerebral ischemia, coronary heart disease and delayed wound healing.

Angiogenesis is a dynamic and complex process regulated by a very sensitive interplay of different growth factors and inhibitors; the maintenance of their correct balance is essential for the physiological control of blood vessel growth.

The interaction between neoplastic cells and newly formed vessels is one of the fundamental biological events involved in the growth of solid tumor growth and metastases formation. The so-called “angiogenic switch” is an alteration in the balance of pro-angiogenic and anti-angiogenic molecules, with an increase of activators, that can be determined by a local change in the tissue environment, such as hypoxia, low pH, injury, inflammation and metal ions dyshomeostasis.

Angiogenesis is also a prominent feature of brain aging and neurological diseases, either as a pathophysiological factor or as a response to injury. Most cases of Alzheimer’s disease have variable degrees of concomitant vascular pathology, including atherosclerosis, microvascular degeneration, blood–brain barrier dysfunction and cerebral amyloid angiopathy. The increased leakiness in the blood vessels disrupts the blood‐brain barrier and allows unwanted blood products to enter the brain causing the progression of disease pathology and promoting amyloid aggregation. Increased numbers of endothelial cell nuclei and blood vessels have been found postmortem in the substantia nigra of patients affected by Parkinson’s disease.

The interaction between cell growth factors as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), angiopoietin, platelet derived growth factor (PDGF), epidermal growth factor (EGF), angiogenin and their respective receptors constitutes one of the main targets for the design of new drugs in many pathologies,  

As volume 1 of the Special Issue “Angiogenesis in Disease ” has been successful, we will be exploring this issue further in the International Journal of Molecular Sciences (ISSN 1422-0067, IF 5.924, JCR Category Q1). This second Special Issue focuses on the signaling pathways of activators and inhibitors of angiogenesis in pathological conditions as well as to new pharmacological approach based on anti- or pro-angiogenic therapies.

https://www.mdpi.com/journal/ijms/special_issues/Angiogenesis_disease

Dr. Diego La Mendola
Prof. Dr. Claudia Martini
Prof. Dr. Maria Letizia Trincavelli
Guest Editors

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Keywords

  • blood vessels
  • angiogenic factors
  • trophic factors
  • angiogenesis biomarkers
  • signaling
  • cancers
  • neurodegeneration
  • heart diseases

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Published Papers (2 papers)

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Research

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15 pages, 4217 KiB  
Article
Characterization of Diabetic Retinopathy in Two Mouse Models and Response to a Single Injection of Anti-Vascular Endothelial Growth Factor
by Tamar Azrad-Leibovich, Alon Zahavi, Moran Friedman Gohas, Myles Brookman, Orit Barinfeld, Orkun Muhsinoglu, Shalom Michowiz, Dror Fixler and Nitza Goldenberg-Cohen
Int. J. Mol. Sci. 2023, 24(1), 324; https://doi.org/10.3390/ijms24010324 - 25 Dec 2022
Cited by 7 | Viewed by 2494
Abstract
In this study, we characterized diabetic retinopathy in two mouse models and the response to anti-vascular endothelial growth factor (VEGF) injection. The study was conducted in 58 transgenic, non-obese diabetic (NOD) mice with spontaneous type 1 diabetes (n = 30, DMT1-NOD) or chemically [...] Read more.
In this study, we characterized diabetic retinopathy in two mouse models and the response to anti-vascular endothelial growth factor (VEGF) injection. The study was conducted in 58 transgenic, non-obese diabetic (NOD) mice with spontaneous type 1 diabetes (n = 30, DMT1-NOD) or chemically induced (n = 28, streptozotocin, STZ-NOD) type 1 diabetes and 20 transgenic db/db mice with type 2 diabetes (DMT2-db/db); 30 NOD and 8 wild-type mice served as controls. Mice were examined at 21 days for vasculopathy, retinal thickness, and expression of genes involved in oxidative stress, angiogenesis, gliosis, and diabetes. The right eye was histologically examined one week after injection of bevacizumab, ranibizumab, saline, or no treatment. Flat mounts revealed microaneurysms and one apparent area of tufts of neovascularization in the diabetic retina. Immunostaining revealed activation of Müller glia and prominent Müller cells. Mean retinal thickness was greater in diabetic mice. RAGE increased and GFAP decreased in DMT1-NOD mice; GFAP and SOX-9 mildly increased in db/db mice. Anti-VEGF treatment led to reduced retinal thickness. Retinas showed vasculopathy and edema in DMT1-NOD and DMT2-db/db mice and activation of Müller glia in DMT1-NOD mice, with some response to anti-VEGF treatment. Given the similarity of diabetic retinopathy in mice and humans, comparisons of type 1 and type 2 diabetic mouse models may assist in the development of new treatment modalities. Full article
(This article belongs to the Special Issue Angiogenesis in Disease 2.0)
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Review

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18 pages, 1223 KiB  
Review
Immunological Profile of Vasospasm after Subarachnoid Hemorrhage
by Michele Romoli, Fabrizio Giammello, Maria Giulia Mosconi, Antonio De Mase, Giovanna De Marco, Anna Digiovanni, Antonio Ciacciarelli, Raffaele Ornello and Benedetta Storti
Int. J. Mol. Sci. 2023, 24(10), 8856; https://doi.org/10.3390/ijms24108856 - 16 May 2023
Cited by 3 | Viewed by 2437
Abstract
Subarachnoid hemorrhage (SAH) carries high mortality and disability rates, which are substantially driven by complications. Early brain injury and vasospasm can happen after SAH and are crucial events to prevent and treat to improve prognosis. In recent decades, immunological mechanisms have been implicated [...] Read more.
Subarachnoid hemorrhage (SAH) carries high mortality and disability rates, which are substantially driven by complications. Early brain injury and vasospasm can happen after SAH and are crucial events to prevent and treat to improve prognosis. In recent decades, immunological mechanisms have been implicated in SAH complications, with both innate and adaptive immunity involved in mechanisms of damage after SAH. The purpose of this review is to summarize the immunological profile of vasospasm, highlighting the potential implementation of biomarkers for its prediction and management. Overall, the kinetics of central nervous system (CNS) immune invasion and soluble factors’ production critically differs between patients developing vasospasm compared to those not experiencing this complication. In particular, in people developing vasospasm, a neutrophil increase develops in the first minutes to days and pairs with a mild depletion of CD45+ lymphocytes. Cytokine production is boosted early on after SAH, and a steep increase in interleukin-6, metalloproteinase-9 and vascular endothelial growth factor (VEGF) anticipates the development of vasospasm after SAH. We also highlight the role of microglia and the potential influence of genetic polymorphism in the development of vasospasm and SAH-related complications. Full article
(This article belongs to the Special Issue Angiogenesis in Disease 2.0)
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