AMPKα inactivation destabilizes atherosclerotic plaque in streptozotocin-induced diabetic mice through AP-2α/miRNA-124 axis

Abstract

Hyperglycemia reduced collagen synthesis, leading to the formation of unstable atherosclerotic plaque induced by collar placement around carotid in apolipoprotein E knockout mice. Hyperglycemia destabilizes atherosclerotic plaque in vivo through an AMPKα/AP-2α/miRNA-124/P4Hα1-dependent collagen synthesis. Metformin functions as a stabilizer of atherosclerotic plaque to reduce acute coronary accent.

Vitamin B6 inhibits macrophage activation to prevent lipopolysaccharide‐induced acute pneumonia in mice

“…37 Metformin, as an antidietetic drug by activating AMPK, inhibits inflammation induced by LPS in vascular cells. 23,24 In lung, suppressing AMPK aggravates LPS-induced lung injury, hypoxia-induced pulmonary arterial hypertension and endothelial barrier dysfunction. 24 Considering these results, it is out of question that AMPK plays a crucial role in VitB6-inhibited inflammation in macrophage.…”

Endogenous reduction of miR‐185 accelerates cardiac function recovery in mice following myocardial infarction via targeting of cathepsin K

“…MicroRNA is a kind of small, nonprotein‐coding RNA that binds to specific 3′ untranslated regions (3′‐UTR) of mRNA and represses target gene expression through inhibition of translation or transcript degradation . In vascular cells, several microRNAs, such as miR‐126, miR‐217, miR‐10a, miR‐124, etc., have been identified to regulate multiple cellular functions including the glucose and lipid metabolisms, senescence and blood flow . We have previously reported that miR‐15b‐5p regulates collateral artery formation by targeting protein kinase B in endothelial cells and miR‐199 regulates normalise arachidonic acid metabolism in nitrate tolerance by prostaglandin synthase .…”

“…5 In vascular cells, several microRNAs, such as miR-126, miR-217, miR-10a, miR-124, etc., have been identified to regulate multiple cellular functions including the glucose and lipid metabolisms, senescence and blood flow. [6][7][8][9] We have previously reported that miR-15b-5p regulates collateral artery formation by targeting protein kinase B in endothelial cells and miR-199 regulates normalise arachidonic acid metabolism in nitrate tolerance by prostaglandin synthase. 10,11 Interestingly, endogenous expressions of miR-133a and miR-130, are null or very low in quiescent endothelial cells, while their expressions are ectopically induced by risk factors, resulting in endothelial dysfunction.…”

Perillaldehyde prevents the formations of atherosclerotic plaques through recoupling endothelial nitric oxide synthase

“…AMPK, as a regulator/modulator of redox status in vascular cells, 36,37 has been reported to inhibited GTPCH1 protein degradation in endothelial cells. We thought that AMP-activated protein kinase (AMPK) should play an important role in this biological process.…”