Table 1.

A summary of the factors involved in endothelial dysfunction.

Factor	Mechanism	Effect on the Function or Structure of ECs	Potential Therapeutic Property	Ref.
TNF-α	It activates the AGE product/receptor of the AGE (RAGE) and (NFκB) signaling path-way.	It induces the activation of NAD(P)H oxidase and the production of reactive oxidative species	TNF-α can induce the secretion of LIF.	(71, 72)
POMC	It inhibits the ET-converting enzyme in ECs.	It induces migration and tube-forming capability of ECs.	LIF can stimulate POMC expression.	(73, 74)
Endothelial YAP-1	YAP expression can cause cardiomyocyte regeneration through IGF1 and Akt signaling.	It induces microRNA-152, which is effective in proliferation.	YAP-1 induces LIF.	(75, 76)
TGF-β	It activates the ALK-5 and Smad-2/3 pathways.	It increases the production of H2O2 and reduces cellular glutathione stores in ECs.	Transforming growth factor β1 induces leukemia inhibitory factor expression.	(77, 78)
SOCS-3	SOCS-3 may protect endothelium by inhibiting IL-6/STAT-3 signaling.	It inhibits the effect of Ang-II and induces endothelial dysfunction.	SOCS-3 modulates leukemia inhibitory factor signaling.	(79, 80)

LIF, Leukemia inhibitory factor; AGE, Advanced glycation end; AGER, Receptor of AGE; NFkB, Nuclear factor-kB; TNF-α, Tumor necrosis factorα; POMC, Proopiomelanocortin; YAP, Yes-associated protein; IGF, Insulin-like growth factor; TGF-β, Transforming growth factor-beta; SOCS-3, Suppressor of cytokine signaling-3