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Endothelial PPARγ Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK
dc.contributor.author | Uddin M.S. | |
dc.contributor.author | Kabir M.T. | |
dc.contributor.author | Jakaria M. | |
dc.contributor.author | Mamun A.A. | |
dc.contributor.author | Niaz K. | |
dc.contributor.author | Amran M.S. | |
dc.contributor.author | Barreto G.E. | |
dc.contributor.author | Ashraf G.M. | |
dc.date.accessioned | 2020-09-02T22:29:29Z | |
dc.date.available | 2020-09-02T22:29:29Z | |
dc.date.issued | 2019 | |
dc.identifier | 10.1007/s12640-019-00047-5 | |
dc.identifier.citation | 36, 3, 583-601 | |
dc.identifier.issn | 10298428 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/6463 | |
dc.description | Aging plays a significant role in the progression of vascular diseases and vascular dysfunction. Activation of the ADP-ribosylation factor 6 and small GTPases by inflammatory signals may cause vascular permeability and endothelial leakage. Pro-inflammatory molecules have a significant effect on smooth muscle cells (SMC). The migration and proliferation of SMC can be promoted by tumor necrosis factor alpha (TNF-α). TNF-α can also increase oxidative stress in SMCs, which has been identified to persuade DNA damage resulting in apoptosis and cellular senescence. Peroxisome proliferator-activated receptor (PPAR) acts as a ligand-dependent transcription factor and a member of the nuclear receptor superfamily. They play key roles in a wide range of biological processes, including cell differentiation and proliferation, bone formation, cell metabolism, tissue remodeling, insulin sensitivity, and eicosanoid signaling. The PPARγ activation regulates inflammatory responses, which can exert protective effects in the vasculature. In addition, loss of function of PPARγ enhances cardiovascular events and atherosclerosis in the vascular endothelium. This appraisal, therefore, discusses the critical linkage of PPARγ in the inflammatory process and highlights a crucial defensive role for endothelial PPARγ in vascular dysfunction and disease, as well as therapy for vascular aging. © 2019, Springer Science+Business Media, LLC, part of Springer Nature. | |
dc.language.iso | en | |
dc.publisher | Springer New York LLC | |
dc.subject | Aging | |
dc.subject | Inflammation | |
dc.subject | Oxidative stress | |
dc.subject | PPARγ | |
dc.subject | ROCK | |
dc.subject | Vascular dysfunction | |
dc.subject | epidermal growth factor | |
dc.subject | hydroxymethylglutaryl coenzyme A reductase kinase | |
dc.subject | icosanoid | |
dc.subject | immunoglobulin enhancer binding protein | |
dc.subject | inducible nitric oxide synthase | |
dc.subject | interleukin 10 | |
dc.subject | interleukin 12 | |
dc.subject | interleukin 1beta | |
dc.subject | interleukin 2 | |
dc.subject | interleukin 6 | |
dc.subject | interleukin 7 | |
dc.subject | interleukin 8 | |
dc.subject | liver X receptor alpha | |
dc.subject | mitogen activated protein kinase 1 | |
dc.subject | mitogen activated protein kinase 3 | |
dc.subject | mitogen activated protein kinase p38 | |
dc.subject | peroxisome proliferator activated receptor delta | |
dc.subject | peroxisome proliferator activated receptor gamma | |
dc.subject | peroxisome proliferator activated receptor gamma 1 | |
dc.subject | peroxisome proliferator activated receptor gamma 2 | |
dc.subject | phosphatidylinositol 3 kinase | |
dc.subject | platelet derived growth factor | |
dc.subject | protein kinase B | |
dc.subject | retinoid X receptor | |
dc.subject | Rho kinase | |
dc.subject | toll like receptor 4 | |
dc.subject | transcription factor AP 1 | |
dc.subject | transforming growth factor beta1 | |
dc.subject | tumor necrosis factor | |
dc.subject | unclassified drug | |
dc.subject | unindexed drug | |
dc.subject | peroxisome proliferator activated receptor gamma | |
dc.subject | Rho kinase | |
dc.subject | aging | |
dc.subject | apoptosis | |
dc.subject | cell differentiation | |
dc.subject | cell metabolism | |
dc.subject | cell migration | |
dc.subject | cell proliferation | |
dc.subject | Crohn disease | |
dc.subject | cytokine production | |
dc.subject | cytokine release | |
dc.subject | disease duration | |
dc.subject | disease severity | |
dc.subject | DNA damage | |
dc.subject | endothelial dysfunction | |
dc.subject | enzyme activation | |
dc.subject | enzyme inhibition | |
dc.subject | enzyme mechanism | |
dc.subject | gene repression | |
dc.subject | human | |
dc.subject | insulin sensitivity | |
dc.subject | multiple sclerosis | |
dc.subject | nonhuman | |
dc.subject | oxidative stress | |
dc.subject | priority journal | |
dc.subject | protein expression | |
dc.subject | protein function | |
dc.subject | protein phosphorylation | |
dc.subject | Review | |
dc.subject | signal transduction | |
dc.subject | single nucleotide polymorphism | |
dc.subject | smooth muscle cell | |
dc.subject | sumoylation | |
dc.subject | Th17 cell | |
dc.subject | ulcerative colitis | |
dc.subject | animal | |
dc.subject | metabolism | |
dc.subject | pathophysiology | |
dc.subject | physiology | |
dc.subject | vascular endothelium | |
dc.subject | Aging | |
dc.subject | Animals | |
dc.subject | Endothelium, Vascular | |
dc.subject | Humans | |
dc.subject | Oxidative Stress | |
dc.subject | PPAR gamma | |
dc.subject | rho-Associated Kinases | |
dc.title | Endothelial PPARγ Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK | |
dc.type | Review |