2022
DOI: 10.1016/j.ejphar.2022.175274
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Transcription factor EB protects against endoplasmic reticulum stress in human coronary artery endothelial cells

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Cited by 8 publications
(2 citation statements)
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“…Lysosomal stress can also activate transcription factor EB (TFEB), which acts as a main regulator of lysosomal biogenesis and function [55]. TFEB is regulated by multiple signaling pathways and can modulate several processes that are important in atherosclerosis, including lipophagy, autophagy, lipolysis, and inflammation [56][57][58][59][60][61]. Thus, lysosomal biogenesis in macrophages stimulated by TFEB may serve as a protective factor for atherosclerosis [62].…”
Section: Lysosomal Dysfunction In Atherosclerosismentioning
confidence: 99%
“…Lysosomal stress can also activate transcription factor EB (TFEB), which acts as a main regulator of lysosomal biogenesis and function [55]. TFEB is regulated by multiple signaling pathways and can modulate several processes that are important in atherosclerosis, including lipophagy, autophagy, lipolysis, and inflammation [56][57][58][59][60][61]. Thus, lysosomal biogenesis in macrophages stimulated by TFEB may serve as a protective factor for atherosclerosis [62].…”
Section: Lysosomal Dysfunction In Atherosclerosismentioning
confidence: 99%
“…Te ER stress is mediated by three unfolded protein response (UPR) mediators [10][11][12][13]. Inositol requiring enzyme 1α (IRE1α), protein kinase RNA-like endoplasmic reticulum kinase (PERK), and activating transcription factor 6 (ATF6) are all localized to the ER membrane and associate with glucose regulated protein 78 (GRP78), an ER-resident molecular chaperone [10].…”
Section: Introductionmentioning
confidence: 99%