Angiogenesis plays a crucial role in the pathophysiology of autoimmune diseases and cancer. Despite the profound differences between these diseases, angiogenesis is a common denominator, which is driven by the immune components of the tissue/tumor microenvironment, in particular via macrophages and neutrophils who act as the main producers of pro-angiogenic mediators. However, angiogenesis has been mostly studied in solid tumors thus far. The complex interplay between tissue cells, endothelial cells and immune cells (especially macrophages) leads to induced production of many pro-angiogenic mediators. Those include, among others, growth factors (e.g., VEGF, PDGF, IGF), matrix degrading enzymes (e.g. matrix metalloproteinases, MMPs), as well as inflammatory mediators and immune modulators (e.g., nitric oxide, TNFa, IL-1ß and chitinase-like proteins-CLPs). These molecules represent potential targets for therapeutic intervention designed to reduce angiogenesis and to block disease progression.
Targeting angiogenesis has been one of the major goals for the treatment of cancer, autoimmune diseases and their vascular complications. Many therapeutics have already been clinically tested, such as the monoclonal antibody bevacizumab (anti-VEGF) and the receptor tyrosine kinase inhibitor, sunitinib. Other novel therapeutics are currently at the pre-clinical stage of investigation.
In this Research Topic, we seek to understand (i) the immunological mechanisms activated by these various therapeutic interventions; (ii) how compensatory mechanisms mediate resistance to these therapeutics; (iii) why some interventions show only limited efficacy (iv) what lessons can be learnt from previous failures, and conversely, (v) what new potential targets and approaches of blocking angiogenesis are now emerging. We welcome the submission of Reviews, Mini-Reviews and Original Research articles that cover, but are not limited to, the following topics, relating to cancer, autoimmune diseases and their complications:
1. Novel immune cell-derived pro-angiogenic targets for blocking angiogenesis.
2. Novel drugs to block previously identified pro-angiogenic targets.
3. Targeting immune cell-derived pro-angiogenic mediators by small molecule inhibitors.
4. Targeting pro-angiogenic mediators by vaccination.
5. Targeting microRNA(s) that regulate immune cell-derived mediators of angiogenesis.
6. Targeting pro-angiogenic mediators in combination with other therapies.
7. Failed targets and lessons learnt in designing therapeutic strategies.
8. Combination of therapies to target angiogenic mediators.
Angiogenesis plays a crucial role in the pathophysiology of autoimmune diseases and cancer. Despite the profound differences between these diseases, angiogenesis is a common denominator, which is driven by the immune components of the tissue/tumor microenvironment, in particular via macrophages and neutrophils who act as the main producers of pro-angiogenic mediators. However, angiogenesis has been mostly studied in solid tumors thus far. The complex interplay between tissue cells, endothelial cells and immune cells (especially macrophages) leads to induced production of many pro-angiogenic mediators. Those include, among others, growth factors (e.g., VEGF, PDGF, IGF), matrix degrading enzymes (e.g. matrix metalloproteinases, MMPs), as well as inflammatory mediators and immune modulators (e.g., nitric oxide, TNFa, IL-1ß and chitinase-like proteins-CLPs). These molecules represent potential targets for therapeutic intervention designed to reduce angiogenesis and to block disease progression.
Targeting angiogenesis has been one of the major goals for the treatment of cancer, autoimmune diseases and their vascular complications. Many therapeutics have already been clinically tested, such as the monoclonal antibody bevacizumab (anti-VEGF) and the receptor tyrosine kinase inhibitor, sunitinib. Other novel therapeutics are currently at the pre-clinical stage of investigation.
In this Research Topic, we seek to understand (i) the immunological mechanisms activated by these various therapeutic interventions; (ii) how compensatory mechanisms mediate resistance to these therapeutics; (iii) why some interventions show only limited efficacy (iv) what lessons can be learnt from previous failures, and conversely, (v) what new potential targets and approaches of blocking angiogenesis are now emerging. We welcome the submission of Reviews, Mini-Reviews and Original Research articles that cover, but are not limited to, the following topics, relating to cancer, autoimmune diseases and their complications:
1. Novel immune cell-derived pro-angiogenic targets for blocking angiogenesis.
2. Novel drugs to block previously identified pro-angiogenic targets.
3. Targeting immune cell-derived pro-angiogenic mediators by small molecule inhibitors.
4. Targeting pro-angiogenic mediators by vaccination.
5. Targeting microRNA(s) that regulate immune cell-derived mediators of angiogenesis.
6. Targeting pro-angiogenic mediators in combination with other therapies.
7. Failed targets and lessons learnt in designing therapeutic strategies.
8. Combination of therapies to target angiogenic mediators.
