**1. Introduction**

The normal vascular endothelium is taken as a gatekeeper of cardiovascular health, whereas abnormality of vascular endothelium is a major contributor to a plethora of cardiovascular ailments, such as atherosclerosis, hypertension, myocardial infarction, coronary artery disease [1]. Therefore, it is important to study the occurrence and development mechanism of vascular endothelial injury. Recent studies have shown that alterations in expression, distribution, and structure of endothelial tight junctions (TJ) may lead to atherosclerosis, neurodegenerative diseases, and pulmonary hypertension, suggesting that TJs play an important role in the vascular endothelium [2].

Occludin, the most representative tight junction proteins, can control the permeability of cells by regulating the connection between cells to play a barrier function. Occludin is involved in the formation of cell polarity *via* forming a fence to prevent cells from spreading to the top and base outer membranes [3]. Meanwhile, occludin can promote cell proliferation and migration [4]. In addition, the expression level of occludin in different vascular beds is positively correlated with the properties of the endothelial barrier of the vascular beds. For example, the permeability of the arterial vascular endothelial barrier is lower than that of the venous vascular endothelial barrier, and the expression of occludin in arterial vascular endothelial is about 18 times higher than that in the venous blood vessels [3], suggesting that occludin is a critical factor of cell permeability and plays an important role in maintaining vascular homeostasis.

Alterations in occludin expression play an important role in vascular endothelial dysfunction. For example, the expression of occludin in retinal vascular endothelial cells of diabetics decreased, resulting in vascular dysfunction such as vascular permeability increased, new vascular formation disorders, and inflammatory response increased, suggesting that the decreased level of occludin may be one of the factors for vascular dysfunction in diabetes [5]. Liu et al. [6] isolated primary mouse retinal endothelial cells for *in vitro* culture and found that occludin S490 phosphorylation is one of the important conditions for retinal endothelial cell tube formation, cell proliferation, and migration. In addition, in the rat with cerebral ischemia at 24 h and 72 h, the expression of occludin in the blood-brain barrier first increased and then decreased [7]. In view of this, understanding the role and mechanism of occludin in vascular endothelial protection is significant for the prevention, diagnosis, and treatment of cardiovascular diseases. We will summarize recent advances in the relationship between occludin and vascular endothelial injury based on the biological information of occludin, the signaling pathway of occludin to protect the vascular endothelium, and the relationship between occludin and vascular endothelial injuryrelated diseases in this chapter.
