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Masayuki Orimo

Researcher at Chiba University

Publications -  6
Citations -  2147

Masayuki Orimo is an academic researcher from Chiba University. The author has contributed to research in topics: Senescence & Vascular endothelial growth factor C. The author has an hindex of 6, co-authored 6 publications receiving 1911 citations. Previous affiliations of Masayuki Orimo include Kanazawa University.

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p53-induced inhibition of Hif-1 causes cardiac dysfunction during pressure overload

TL;DR: It is shown that cardiac angiogenesis is crucially involved in the adaptive mechanism of cardiachypertrophy and that p53 accumulation is essential for the transition from cardiac hypertrophy to heart failure and that the anti-angiogenic property of p53 may have a crucial function in the transition.
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A crucial role for adipose tissue p53 in the regulation of insulin resistance

TL;DR: It is shown that p53 expression in adipose tissue is crucially involved in the development of insulin resistance, which underlies age-related cardiovascular and metabolic disorders and suggests that cellular aging signals in adipOSE tissue could be a new target for the treatment of diabetes.
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Angiotensin II Induces Premature Senescence of Vascular Smooth Muscle Cells and Accelerates the Development of Atherosclerosis via a p21-Dependent Pathway

TL;DR: The results suggest a critical role of p21-dependent premature senescence of VSMCs in the pathogenesis of atherosclerosis, and demonstrate that Ang II promotes vascular inflammation by inducing premature senesence ofVSMCs both in vitro and in vivo.
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Protective Role of SIRT1 in Diabetic Vascular Dysfunction

TL;DR: These findings represent a novel mechanism of vascular cell senescence induced by hyperglycemia and suggest a protective role of SIRT1 in the pathogenesis of diabetic vasculopathy.
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Cellular Senescence Impairs Circadian Expression of Clock Genes In Vitro and In Vivo

TL;DR: The results suggest that senescence decreases the ability of cells to transmit circadian signals to their clocks and that regulation of clock gene expression may be a novel strategy for the treatment of age-associated impairment of circadian rhythmicity.