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Fig. 7 | Cardiovascular Diabetology

Fig. 7

From: MicroRNAs and obesity-induced endothelial dysfunction: key paradigms in molecular therapy

Fig. 7

Obesity, ER stress, miRNAs and endothelial function. Under ER stress, BIP will activate the three UPR sensor pathways that are initiated by PERK, ATF6, and IRE1. MicroRNAs involved in the UPR pathway and evidenced linkage to obesity and endothelial dysfunction are listed in this diagram. miR-30d, miR-181a, and miR-199a-5p have all been shown to directly target BIP. MiR-204, miR-23a, miR-27a and miR-24 directly target and inhibit PERK signaling, which then causes ER-stress-induced cell death. ATF4, located downstream of PERK, is directly inhibited by miR-214 and miR-663. CHOP, which is regulated by ATF4, is suppressed by miR-211. IRE1α and its downstream signaling XBP1 make up the second arm of the UPR; the former is targeted by miR-1291, miR-23a, miR-27a and miR-24, while the latter is targeted by miR-214. Finally, in the third arm of UPR, miR-221, miR-145 and miR-494 directly target ATF6. ER: endoplasmic reticulum; ATF6: Activating transcription factor 6; IRE1α inositol requiring enzyme 1 alpha; and PERK protein kinase-like ER kinase; BIP: Binding Immunoglobulin Protein, also known as GRP78; UPR: unfolded protein response, ATF 4: Activating transcription factor 4; CHOP: CCAAT-enhancer-binding protein homologous protein; XBP1: X box binding protein 1; EI2 α: Eukaryotic Initiation Factor 2 alpha

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