Pioglitazone, a PPARγ agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling. (Q36578665)

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scientific article published on 28 November 2015

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English	Pioglitazone, a PPARγ agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling.	scientific article published on 28 November 2015

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scholarly article

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2 March 2020

Pioglitazone, a PPARγ agonist, attenuates PDGF-induced vascular smooth muscle cell proliferation through AMPK-dependent and AMPK-independent inhibition of mTOR/p70S6K and ERK signaling (English)

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Lakshman Segar

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28 November 2015

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Biochemical Pharmacology

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2 March 2020

Metformin exaggerates phenylephrine-induced AMPK phosphorylation independent of CaMKKβ and attenuates contractile response in endothelium-denuded rat aorta

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RORα suppresses proliferation of vascular smooth muscle cells through activation of AMP-activated protein kinase

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mTOR inhibition: a promising strategy for stabilization of atherosclerotic plaques

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AMP is a true physiological regulator of AMP-activated protein kinase by both allosteric activation and enhancing net phosphorylation

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Expression of conventional and novel glucose transporters, GLUT1, -9, -10, and -12, in vascular smooth muscle cells

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AMP-activated protein kinase inhibits vascular smooth muscle cell proliferation and migration and vascular remodeling following injury

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PDGF-induced vascular smooth muscle cell proliferation is associated with dysregulation of insulin receptor substrates

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Pioglitazone-induced reductions in atherosclerosis occur via smooth muscle cell-specific interaction with PPAR{gamma}.

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Molecular mechanisms of mTOR-mediated translational control

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Dominant-negative loss of PPARgamma function enhances smooth muscle cell proliferation, migration, and vascular remodeling.

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Pioglitazone stimulates AMP-activated protein kinase signalling and increases the expression of genes involved in adiponectin signalling, mitochondrial function and fat oxidation in human skeletal muscle in vivo: a randomised trial

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AMPK phosphorylation of raptor mediates a metabolic checkpoint

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Pioglitazone and risk of cardiovascular events in patients with type 2 diabetes mellitus: a meta-analysis of randomized trials

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Glycemic durability of rosiglitazone, metformin, or glyburide monotherapy

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Secondary prevention of macrovascular events in patients with type 2 diabetes in the PROactive Study (PROspective pioglitAzone Clinical Trial In macroVascular Events): a randomised controlled trial

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Thiazolidinedione use, fluid retention, and congestive heart failure: a consensus statement from the American Heart Association and American Diabetes Association. October 7, 2003.

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Rosiglitazone reduces the accelerated neointima formation after arterial injury in a mouse injury model of type 2 diabetes

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Adipocyte-derived plasma protein adiponectin acts as a platelet-derived growth factor-BB-binding protein and regulates growth factor-induced common postreceptor signal in vascular smooth muscle cell

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The Anti-diabetic drugs rosiglitazone and metformin stimulate AMP-activated protein kinase through distinct signaling pathways.

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PPARgamma and atherosclerosis: effects on cell growth and movement

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Peroxisome proliferator-activated receptor (PPAR)-gamma expression in human vascular smooth muscle cells: inhibition of growth, migration, and c-fos expression by the peroxisome proliferator-activated receptor (PPAR)-gamma activator troglitazone

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Troglitazone inhibits vascular smooth muscle cell growth and intimal hyperplasia

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Troglitazone causes acute mitochondrial membrane depolarisation and an AMPK-mediated increase in glucose phosphorylation in muscle cells.

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Adiponectin induces vascular smooth muscle cell differentiation via repression of mammalian target of rapamycin complex 1 and FoxO4.

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Pioglitazone treatment activates AMP-activated protein kinase in rat liver and adipose tissue in vivo

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Differential effects of the cyclin-dependent kinase inhibitors p27(Kip1), p21(Cip1), and p16(Ink4) on vascular smooth muscle cell proliferation.

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Expression and function of PPARgamma in rat and human vascular smooth muscle cells

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Activation of human aortic smooth-muscle cells is inhibited by PPARalpha but not by PPARgamma activators.

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AMP-activated protein kinase inhibits angiotensin II-stimulated vascular smooth muscle cell proliferation

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Differential inhibitory effects of antidiabetic drugs on arterial smooth muscle cell proliferation

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12 December 2020

based on heuristic

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Vasculo-protective effects of insulin sensitizing agent pioglitazone in neointimal thickening and hypertensive vascular hypertrophy

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https://pubmed.ncbi.nlm.nih.gov/26643070

12 December 2020

based on heuristic

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Adipose-derived protein omentin prevents neointimal formation after arterial injury

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12 December 2020

based on heuristic

inferred from PubMed ID database lookup

Identifiers

10.1016/J.BCP.2015.11.026

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Europe PubMed Central

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2 March 2020

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Europe PubMed Central

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2 March 2020

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2 March 2020

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