Endothelial PPAR gamma Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK

Uddin M.S.; Kabir M.T.; Jakaria M.; Mamun A.A.; Niaz K.; Amran M.S.; Barreto G.E.; Ashraf G.M.

Abstract

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-alpha). TNF-alpha 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 PPAR gamma activation regulates inflammatory responses, which can exert protective effects in the vasculature. In addition, loss of function of PPAR gamma enhances cardiovascular events and atherosclerosis in the vascular endothelium. This appraisal, therefore, discusses the critical linkage of PPAR gamma in the inflammatory process and highlights a crucial defensive role for endothelial PPAR gamma in vascular dysfunction and disease, as well as therapy for vascular aging.

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Título según WOS: Endothelial PPAR gamma Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK
Título según SCOPUS: Endothelial PPAR? Is Crucial for Averting Age-Related Vascular Dysfunction by Stalling Oxidative Stress and ROCK
Título de la Revista: NEUROTOXICITY RESEARCH
Volumen: 36
Número: 3
Editorial: Springer
Fecha de publicación: 2019
Página de inicio: 583
Página final: 601
Idioma: English
DOI:

10.1007/s12640-019-00047-5

Notas: ISI, SCOPUS