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. 2022 Apr 16;2022:3311228. doi: 10.1155/2022/3311228

Table 1.

Summary of the type of endothelial cell damaging factors with its effects on respective vascular endothelial cells.

Source Type of endothelial cell Effect/mechanism Ref.
Tumor necrosis factor-alpha (TNF-α) Human umbilical vein endothelial cells (HUVECs) (i) Induction of oxidative stress, inflammation, and apoptosis
(ii) Induction of inflammation and monocytes adhesion
[28,29]
Glycated low-density lipoprotein (glyLDL) Porcine aortic EC (PAEC) (i) Induction of oxidative stress and apoptosis [30]
Bradykinin HUVECs (i) Induction of endothelial hyperpermeability
(ii) Stimulation of angiogenesis via increased endothelial permeability and remodeling
[31,32]
Histamine HUVEC
Human dermal microvascular endothelial cells (HDMEC)
(i) Increased endothelial permeability through PLC-NO-cGMP signaling cascade
(ii) Induction of endothelial dysfunction by activating Ca2+-mediated RhoA and adherens junctions' tension
[33,34]
α-Thrombin HUVECs (i) Increased endothelial macromolecular permeability [35]
IFNγ HUVEC (i) Induction of endothelial hyperpermeability via activation of p38 MAP kinase and actin cytoskeleton alteration [36]
IL-1α Brain microvascular endothelial cells (BECs) Activation and induction of angiogenic markers in endothelial cells [37]
IL-1β Human glomerular endothelial cell (HRGEC) Induction of vascular hyperpermeability and upregulation of vascular endothelial-cadherin [38]
IL-4 Human coronary artery endothelial cells (HCAEC) and human pulmonary artery endothelial cells (HPAEC) Induction of vascular hyperpermeability through Wnt5A signaling [39]
Lipopolysaccharide (LPS) HUVECs
HUVECs and human lung microvascular endothelial cells (HMVEC-L)
(i) Induction of apoptosis, injury, JNK phosphorylation, decreased MCL-1 expression and SOD activity, and increased proinflammatory cytokine production.
(ii) Activation of endothelial cells' inflammatory responses
[40,41]
Thrombin Primary human dermal microvascular endothelial cells (HDMECs) 
Human pulmonary microvascular endothelial cells (HPMVECs)
(i) Induction of microvessel leakage
(ii) Induction of vascular hyperpermeability via dysregulation of vascular endothelial (VE-)cadherin and alteration of small rho GTPases
[42,43]
Angiotensin II (Ang II) HUVECs Induced vascular endothelial cells' injury and oxidative stress [44]
Glucose Rat aortic endothelial cells (RAOECs) Induces cyclin D2 upregulation and miR‐98 downregulation [45]