Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Biochemistry & Molecular Biology, Biophysics, Cell Biology, autophagy, cancer, endothelial cells, immunosurveillance, tumor vasculature, LC3-ASSOCIATED PHAGOCYTOSIS, TUMOR VASCULATURE, OXIDATIVE STRESS, NITRIC-OXIDE, GROWTH, NORMALIZATION, MITOCHONDRIA, ACTIVATION, MELANOMA, HYPOXIA, Animals, Autophagy, Autophagy-Related Proteins, Blood Vessels, Cytokines, Endothelial Cells, Gene Expression Regulation, Neoplastic, Homeostasis, Humans, Hypoxia, Immunologic Surveillance, Lysosomes, Neoplasms, Neovascularization, Pathologic, Signal Transduction, Tumor Microenvironment, Cancer, Endothelial cells, Immunosurveillance, Tumor vasculature, 0304 Medicinal and Biomolecular Chemistry, 0601 Biochemistry and Cell Biology, 0603 Evolutionary Biology, 3101 Biochemistry and cell biology

Abstract:

Autophagy, the major lysosomal pathway for the degradation and recycling of cytoplasmic materials, is increasingly recognized as a major player in endothelial cell (EC) biology and vascular pathology. Particularly in solid tumors, tumor microenvironmental stress such as hypoxia, nutrient deprivation, inflammatory mediators, and metabolic aberrations stimulates autophagy in tumor-associated blood vessels. Increased autophagy in ECs may serve as a mechanism to alleviate stress and restrict exacerbated inflammatory responses. However, increased autophagy in tumor-associated ECs can re-model metabolic pathways and affect the trafficking and surface availability of key mediators and regulators of the interplay between EC and immune cells. In line with this, heightened EC autophagy is involved in pathological angiogenesis, inflammatory, and immune responses. Here, we review major cellular and molecular mechanisms regulated by autophagy in ECs under physiological conditions and discuss recent evidence implicating EC autophagy in tumor angiogenesis and immunosurveillance.