Table 3.

Altered NFAT5 expression and cardiovascular dysfunction.

Cardiovascular Dysfunction	Cell Type or Model	Altered NFAT5 Expression and Consequences	Reference
Dox-induced cytotoxicity	Cardiomyocytes	Dox promotes NFAT5 degradation, leading to downregulated TauT expression and cardiomyocyte injury.	[88,89,90]
Myocardial infarction	Cultured cardiomyocytes, cardiac macrophages	Hypertonicity upregulates NFAT5 to induce downstream target gene expression; NFAT is involved in activating macrophages to exacerbate postinfarction damage.	[91,92]
Arterial wall stress	VSMC, mice	Biomechanical stretching upregulates NFAT5 to influence downstream target genes, such as tenascin-C and κ-actin, in arterial remodelling and VSMC migration.	[11,93,94]
Atherosclerosis	VSMC, mice	NFAT5 converts VSMC to the contractile and migratory phenotypes after ANG II and PDGF-BB stimulation, respectively.	[95]
	Macrophages	NFAT5 is involved in macrophage chemotactic migration by M-CSF stimulation.	[96]
	Human umbilical vein endothelial cells, rat	NFAT5 promotes arteriogenesis and angiogenesis by MCP-1 monocyte recruitment.	[97]
	Mouse, human umbilical vein endothelial cells and monocytes	NLRP3 inflammasome activation by NFAT5 increases IL-1b expression to facilitate inflammation in endothelial cells and recruit monocytes.	[98]
	Macrophages	VEGF-C upregulation is protective against salt-induced hypertension and stimulates eNOS to protect blood pressure homeostasis. VEGF-C upregulation stimulates intimal neovascularization and enhances atherosclerotic lesion progression.	[95,99]