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Targeting Blood Vessels in Cancer and Fibrosis

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: 30 May 2024 | Viewed by 645

Special Issue Editor

Departamento de Bioquímica y Biología Molecular, Universidad de Salamanca, Salamanca, Spain
Interests: tumor angiogenesis; vessel co-option; lung metastases; tissue fibrosis; pericytes
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Blood vessels are tubes that carry blood throughout an organism. Blood supplies oxygen and nutrients to different tissues. Changes in blood vessels occur in different pathologies such as cancer or tissue fibrosis. Tumors need the formation of a fine network of blood vessels to provide nutrients to cancer cells. However, tumor vasculature is normally immature and leaky and generates hypoxia in tumor cells that mediate therapy resistance and metastasis. For this reason, the modulation of tumor vasculature using different strategies such as anti-angiogenesis or vessel normalization is an interesting approach to enhance the efficacy of cancer therapy. Fibrotic diseases in organs such as the lungs, liver, heart or kidneys are characterized by the accumulation of extracellular matrices in the tissue parenchyma and microvascular rarefaction that also lead to tissue hypoxia. The modulation of microvasculature in fibrotic tissues to eliminate hypoxia and control the buildup of extracellular matrix is also being explored.

This Special Issue welcomes original articles and reviews focused on the novelties in the modulation of blood vessels in cancer and fibrotic diseases.

Dr. José M. Muñoz-Félix
Guest Editor

Manuscript Submission Information

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Keywords

  • blood vessels
  • angiogenesis
  • fibrosis
  • fibroblasts
  • hypoxia
  • pericytes

Published Papers (1 paper)

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Review

27 pages, 2650 KiB  
Review
The Inhibition of Vessel Co-Option as an Emerging Strategy for Cancer Therapy
Int. J. Mol. Sci. 2024, 25(2), 921; https://doi.org/10.3390/ijms25020921 - 11 Jan 2024
Viewed by 546
Abstract
Vessel co-option (VCO) is a non-angiogenic mechanism of vascularization that has been associated to anti-angiogenic therapy. In VCO, cancer cells hijack the pre-existing blood vessels and use them to obtain oxygen and nutrients and invade adjacent tissue. Multiple primary tumors and metastases undergo [...] Read more.
Vessel co-option (VCO) is a non-angiogenic mechanism of vascularization that has been associated to anti-angiogenic therapy. In VCO, cancer cells hijack the pre-existing blood vessels and use them to obtain oxygen and nutrients and invade adjacent tissue. Multiple primary tumors and metastases undergo VCO in highly vascularized tissues such as the lungs, liver or brain. VCO has been associated with a worse prognosis. The cellular and molecular mechanisms that undergo VCO are poorly understood. Recent studies have demonstrated that co-opted vessels show a quiescent phenotype in contrast to angiogenic tumor blood vessels. On the other hand, it is believed that during VCO, cancer cells are adhered to basement membrane from pre-existing blood vessels by using integrins, show enhanced motility and a mesenchymal phenotype. Other components of the tumor microenvironment (TME) such as extracellular matrix, immune cells or extracellular vesicles play important roles in vessel co-option maintenance. There are no strategies to inhibit VCO, and thus, to eliminate resistance to anti-angiogenic therapy. This review summarizes all the molecular mechanisms involved in vessel co-option analyzing the possible therapeutic strategies to inhibit this process. Full article
(This article belongs to the Special Issue Targeting Blood Vessels in Cancer and Fibrosis)
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