Interstitial lung disease (ILD) encompasses a group of heterogeneous diseases characterised by varying degrees of aberrant inflammation and fibrosis of the lung parenchyma. This may occur in isolation, such as in idiopathic pulmonary fibrosis (IPF) or as part of a wider disease process affecting multiple organs, such as in systemic sclerosis. Anti-Vascular Endothelial Growth Factor (anti-VEGF) therapy is one component of an existing broad-spectrum therapeutic option in IPF (nintedanib) and may become part of the emerging therapeutic strategy for other ILDs in the future. This article describes our current understanding of VEGF biology in normal lung homeostasis and how changes in its bioavailability may contribute the pathogenesis of ILD. The complexity of VEGF biology is particularly highlighted with an emphasis on the potential non-vascular, non-angiogenic roles for VEGF in the lung, in both health and disease.
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http://dx.doi.org/10.3390/ijms19051269 | DOI Listing |
Adv Sci (Weinh)
January 2025
Eye Center, The Second Affiliated Hospital, School of Medicine, Zhejiang Provincial Key Laboratory of Ophthalmology, Zhejiang Provincial Clinical Research Center for Eye Diseases, Zhejiang Provincial Engineering Institute on Eye Diseases, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, China.
Age-related macular degeneration (AMD), characterized by choroidal neovascularization (CNV), is the global leading cause of irreversible blindness. Current first-line therapeutics, vascular endothelial growth factor (VEGF) antagonists, often yield incomplete and suboptimal vision improvement, necessitating the exploration of novel and efficacious therapeutic approaches. Herein, a supramolecular engineering strategy to construct moringin (MOR) loaded α-cyclodextrin (α-CD) coated nanoceria (M@CCNP) is constructed, where the hydroxy and newly formed carbonyl groups of α-CD interact with the nanoceria surface via O─Ce conjunction and the isothiocyanate group of MOR inserts deeply into the α-CD cavity via host-guest interaction.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
ETH Zurich, Department of Biosystems Science and Engineering, Klingelbergstrasse 48, Basel, CH-4056, Switzerland.
Neo-vascularization plays a key role in achieving long-term viability of engineered cells contained in medical implants used in precision medicine. Moreover, strategies to promote neo-vascularization around medical implants may also be useful to promote the healing of deep wounds. In this context, a biocompatible, electroconductive borophene-poly(ε-caprolactone) (PCL) 3D platform is developed, which is called VOLT, to support designer cells engineered with a direct-current (DC) voltage-controlled gene circuit that drives secretion of vascular endothelial growth factor A (VEGFA).
View Article and Find Full Text PDFClin Neuropharmacol
January 2025
Department of Neurosurgery, Yubei District Hospital of TCM, Chongqing, China.
Objective: Gliomas are a general designation for neuroepithelial tumors derived from the glial cells of the central nervous system. According to the histopathological and immunohistochemical features, the World Health Organization classifies gliomas into four grades. Bevacizumab is a monoclonal antibody targeting vascular endothelial growth factor that has been approved for the treatment of glioblastoma multiforme (GBM) as a second-line therapy.
View Article and Find Full Text PDFJ Cancer Res Ther
December 2024
Department of Gastrointestinal Surgery, Guangxi Medical University Cancer Hospital, Nanning, China.
Background: Colorectal cancer (CRC) is one of the most common cancers worldwide. The mechanisms underlying metastasis, which contributes to poor outcomes, remain elusive.
Methods: We used the Cancer Genome Atlas dataset to compare mRNA expression patterns of integrin α6 (ITGA6) and integrin β4 (ITGB4) in patients with CRC.
Transl Vis Sci Technol
January 2025
Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Purpose: Alteration of visual acuity in wet age-related macular degeneration (AMD) is mostly driven by vascular endothelial growth factor A (VEGF-A)-induced edema from leaky newly forming blood vessels below the retina layers. To date, all therapies aimed at alleviation of this process have relied on inhibition of VEGF-A activity. Although effective in preventing vascular leak and edema, this approach also leads to the loss of normal vasculature and multiple related side effects.
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