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dc.contributor.authorUddin M.S.
dc.contributor.authorKabir M.T.
dc.contributor.authorJakaria M.
dc.contributor.authorMamun A.A.
dc.contributor.authorNiaz K.
dc.contributor.authorAmran M.S.
dc.contributor.authorBarreto G.E.
dc.contributor.authorAshraf G.M.
dc.date.accessioned2020-09-02T22:29:29Z
dc.date.available2020-09-02T22:29:29Z
dc.date.issued2019
dc.identifier10.1007/s12640-019-00047-5
dc.identifier.citation36, 3, 583-601
dc.identifier.issn10298428
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6463
dc.descriptionAging 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.isoen
dc.publisherSpringer New York LLC
dc.subjectAging
dc.subjectInflammation
dc.subjectOxidative stress
dc.subjectPPARγ
dc.subjectROCK
dc.subjectVascular dysfunction
dc.subjectepidermal growth factor
dc.subjecthydroxymethylglutaryl coenzyme A reductase kinase
dc.subjecticosanoid
dc.subjectimmunoglobulin enhancer binding protein
dc.subjectinducible nitric oxide synthase
dc.subjectinterleukin 10
dc.subjectinterleukin 12
dc.subjectinterleukin 1beta
dc.subjectinterleukin 2
dc.subjectinterleukin 6
dc.subjectinterleukin 7
dc.subjectinterleukin 8
dc.subjectliver X receptor alpha
dc.subjectmitogen activated protein kinase 1
dc.subjectmitogen activated protein kinase 3
dc.subjectmitogen activated protein kinase p38
dc.subjectperoxisome proliferator activated receptor delta
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectperoxisome proliferator activated receptor gamma 1
dc.subjectperoxisome proliferator activated receptor gamma 2
dc.subjectphosphatidylinositol 3 kinase
dc.subjectplatelet derived growth factor
dc.subjectprotein kinase B
dc.subjectretinoid X receptor
dc.subjectRho kinase
dc.subjecttoll like receptor 4
dc.subjecttranscription factor AP 1
dc.subjecttransforming growth factor beta1
dc.subjecttumor necrosis factor
dc.subjectunclassified drug
dc.subjectunindexed drug
dc.subjectperoxisome proliferator activated receptor gamma
dc.subjectRho kinase
dc.subjectaging
dc.subjectapoptosis
dc.subjectcell differentiation
dc.subjectcell metabolism
dc.subjectcell migration
dc.subjectcell proliferation
dc.subjectCrohn disease
dc.subjectcytokine production
dc.subjectcytokine release
dc.subjectdisease duration
dc.subjectdisease severity
dc.subjectDNA damage
dc.subjectendothelial dysfunction
dc.subjectenzyme activation
dc.subjectenzyme inhibition
dc.subjectenzyme mechanism
dc.subjectgene repression
dc.subjecthuman
dc.subjectinsulin sensitivity
dc.subjectmultiple sclerosis
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein phosphorylation
dc.subjectReview
dc.subjectsignal transduction
dc.subjectsingle nucleotide polymorphism
dc.subjectsmooth muscle cell
dc.subjectsumoylation
dc.subjectTh17 cell
dc.subjectulcerative colitis
dc.subjectanimal
dc.subjectmetabolism
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectvascular endothelium
dc.subjectAging
dc.subjectAnimals
dc.subjectEndothelium, Vascular
dc.subjectHumans
dc.subjectOxidative Stress
dc.subjectPPAR gamma
dc.subjectrho-Associated Kinases
dc.titleEndothelial PPARγ Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK
dc.typeReview


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