2019
DOI: 10.1007/s11033-019-05229-0
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Association between the transporters ABCA1/G1 and the expression of miR-33a/144 and the carotid intima media thickness in patients with arterial hypertension

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Cited by 6 publications
(5 citation statements)
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“…Participants with T-allele (TT + CT) of rs1799858 were not only associated with increased risk of higher LDL-C level but also with increased risk of atherosclerosis events, including carotid artery stenosis (CAS) ≥ 50% and new-onset/recurrent acute myocardial infarction (AMI). Synchronously, the data reported in this study indicated that those DE-exo-miRs between the two genotypes (CC vs. TT + CT) of rs1799858 were not only involved in lipid metabolism/dyslipidemia as mentioned above but also played a pivotal role in the occurrence and progression of arteriosclerosis [27,28], such as miR-22-3p, miR-490-3p, miR-210-3p, miR-497-5p, miR-33a-5p, miR-126-5p, miR-451b, miR-320 family (e.g., miR-320b), miR-208 family (e.g., miR-208b-3p), let-7 family (e.g., let-7i-5p, let-7g-5p, let-7a-5p and let-7f-5p) and miR-221/222 family (e.g., miR-222-3p and miR-221-5p), involving in proliferation and migration of VSMCs (e.g., miR-22-3p [29] and miR-490-3p [18]), ECs dysfunction (e.g., miR-22-3p [30], miR-126 [31], miR-221/222 family [13]), plaque angiogenesis (e.g., miR-126 [32]), apoptosis (e.g., miR-210-3p [33], miR-320d [34]) and macrophage lipid deposition (e.g., miR-210-3p [20]). In particular, miR-483-5p [35], miR-31-5p [36], miR-320b [19] and miR-126 [37] were also closely related to the stenosis degree and unstable phenotype of atherosclerotic plaques, suggesting those exo-miRs may be related to the potential risk of acute vascular events.…”
Section: Discussionsupporting
confidence: 64%
“…Participants with T-allele (TT + CT) of rs1799858 were not only associated with increased risk of higher LDL-C level but also with increased risk of atherosclerosis events, including carotid artery stenosis (CAS) ≥ 50% and new-onset/recurrent acute myocardial infarction (AMI). Synchronously, the data reported in this study indicated that those DE-exo-miRs between the two genotypes (CC vs. TT + CT) of rs1799858 were not only involved in lipid metabolism/dyslipidemia as mentioned above but also played a pivotal role in the occurrence and progression of arteriosclerosis [27,28], such as miR-22-3p, miR-490-3p, miR-210-3p, miR-497-5p, miR-33a-5p, miR-126-5p, miR-451b, miR-320 family (e.g., miR-320b), miR-208 family (e.g., miR-208b-3p), let-7 family (e.g., let-7i-5p, let-7g-5p, let-7a-5p and let-7f-5p) and miR-221/222 family (e.g., miR-222-3p and miR-221-5p), involving in proliferation and migration of VSMCs (e.g., miR-22-3p [29] and miR-490-3p [18]), ECs dysfunction (e.g., miR-22-3p [30], miR-126 [31], miR-221/222 family [13]), plaque angiogenesis (e.g., miR-126 [32]), apoptosis (e.g., miR-210-3p [33], miR-320d [34]) and macrophage lipid deposition (e.g., miR-210-3p [20]). In particular, miR-483-5p [35], miR-31-5p [36], miR-320b [19] and miR-126 [37] were also closely related to the stenosis degree and unstable phenotype of atherosclerotic plaques, suggesting those exo-miRs may be related to the potential risk of acute vascular events.…”
Section: Discussionsupporting
confidence: 64%
“…Therefore , ABCA1 performs a necessary role in mediating cellular cholesterol, phospholipid efflux, and HDL biosynthesis ( 24 ). ABCA1 was an integral membrane protein, which transported excess cholesterol from peripheral tissues to the liver for excretion, by mediating the first step of reverse cholesterol transport (RCT) ( 25 , 26 ). Xu et al verified that cholesterol efflux from monocyte-derived macrophages to autologous serum, HDL was impaired in hypertensive patients, and that ABCA1 expression was associated with this impairment ( 17 ).…”
Section: Discussionmentioning
confidence: 99%
“…ABCA1 mediates the first step of reverse cholesterol transport by transporting excess cholesterol in peripheral tissues to the liver for excretion ( 58 ). Recent evidence has shown that the expression of ABCA1 is significantly decreased in patients with hypertension, and the outflow of cholesterol to apo-A1 leads to increased carotid intima-media thickness, and promotes arterial hypertension ( 59 ). Interestingly, in ESI+/ESI– modes, we identified 19 differential metabolites that were enriched in the metabolic pathway of the ABC transporter.…”
Section: Discussionmentioning
confidence: 99%