2. Academic Validation
  3. E-selectin in vascular pathophysiology

E-selectin in vascular pathophysiology

  • Front Immunol. 2024 Jul 19:15:1401399. doi: 10.3389/fimmu.2024.1401399.
Jinjin Zhang # 1 2,  Shengshi Huang # 3 4,  Zhiying Zhu 1,  Alex Gatt 5 6,  Ju Liu 1 3 4
Affiliations

Affiliations

  • 1 Department of Laboratory Medicine, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
  • 2 Medical Research Center, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan, China.
  • 3 Institute of Microvascular Medicine, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.
  • 4 Shandong Provincial Key Medical and Health Laboratory of Translational Medicine in Microvascular Aging, Jinan, China.
  • 5 Department of Pathology, Faculty of Medicine and Surgery, University of Malta, Msida, Malta.
  • 6 Haematology Laboratory, Department of Pathology, Mater Dei Hospital, Msida, Malta.
  • # Contributed equally.
PMID: 39100681 DOI: 10.3389/fimmu.2024.1401399
Abstract

Selectins are a group of CA2+-dependent, transmembrane type I glycoproteins which attract cell adhesion and migration. E-Selectin is exclusively expressed in endothelial cells, and its expression is strongly enhanced upon activation by pro-inflammatory cytokines. The interaction of E-Selectin with its ligands on circulating leukocytes captures and slows them down, further facilitating Integrin activation, firm adhesion to endothelial cells and transmigration to tissues. Oxidative stress induces endothelial cell injury, leading to aberrant expression of E-Selectin. In addition, the elevated level of E-Selectin is positively related to high risk of inflammation. Dysregulation of E-Selectin has been found in several pathological conditions including acute kidney injury (AKI), pulmonary diseases, hepatic pathology, Venous thromboembolism (VTE). Deletion of the E-Selectin gene in mice somewhat ameliorates these complications. In this review, we describe the mechanisms regulating E-Selectin expression, the interaction of E-Selectin with its ligands, the E-Selectin physiological and pathophysiological roles, and the therapeutical potential of targeting E-Selectin.

Keywords

E-selectin; inflammation; oxidative stress; therapeutic interventions; vascular diseases.

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