Emerging Role of IRE1α in Vascular Diseases
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Abstract
A mounting body of evidence suggests that the endoplasmic reticulum stress and the unfolded protein response are involved in the underlying mechanisms responsible for vascular diseases. Inositol-requiring protein 1α (IRE1α), the most ancient branch among the UPR-related signaling pathways, can possess both serine/threonine kinase and endoribonuclease (RNase) activity and can perform physiological and pathological functions. The IRE1α-signaling pathway plays a critical role in the pathology of various vascular diseases. In this review, we provide a general overview of the physiological function of IRE1α and its pathophysiological role in vascular diseases.
References
1.
McMonagle M
. The quest for effective pharmacological suppression of neointimal hyperplasia. Curr Probl Surg. 2020; 57(8):100807.
DOI: 10.1016/j.cpsurg.2020.100807.
View
2.
Margariti A, Li H, Chen T, Martin D, Vizcay-Barrena G, Alam S
. XBP1 mRNA splicing triggers an autophagic response in endothelial cells through BECLIN-1 transcriptional activation. J Biol Chem. 2012; 288(2):859-72.
PMC: 3543035.
DOI: 10.1074/jbc.M112.412783.
View
3.
. Global, regional, and national age-sex-specific mortality for 282 causes of death in 195 countries and territories, 1980-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018; 392(10159):1736-1788.
PMC: 6227606.
DOI: 10.1016/S0140-6736(18)32203-7.
View
4.
Kim T, Lee S, Kim M, Cheon C, Ko S
. Kaempferol induces autophagic cell death via IRE1-JNK-CHOP pathway and inhibition of G9a in gastric cancer cells. Cell Death Dis. 2018; 9(9):875.
PMC: 6115440.
DOI: 10.1038/s41419-018-0930-1.
View
5.
Shen Y, Zhao W, Monroig O, Bao Y, Zhu T, Jiao L
. High-fat-diet induced inflammation and apoptosis via activation of Ire1α in liver and hepatocytes of black seabream (Acanthopagrus schlegelii). Fish Shellfish Immunol. 2023; 143:109212.
DOI: 10.1016/j.fsi.2023.109212.
View