Paper
Fenofibrate regulates retinal endothelial cell survival through the AMPK signal transduction pathway.
Published May 1, 2007 · Jaetaek Kim, Jihyun Ahn, Jeong-Hun Kim
Experimental eye research
Q1 SJR score
113
Citations
1
Influential Citations
Abstract
Abstract hidden due to publisher request; this does not indicate any issues with the research. Click the full text link above to read the abstract and view the original source.
In Vitro Study
Highly CitedStudy Snapshot
Fenofibrate protects retinal endothelial cells from apoptosis in response to serum deprivation through a PPARalpha-independent, but AMPK-dependent pathway, potentially offering a novel therapeutic approach for diabetic retinopathy.
PopulationOlder adults (50-71 years)
Sample size24
MethodsObservational
OutcomesBody Mass Index projections
ResultsSocial networks mitigate obesity in older groups.
Full text analysis coming soon...
References
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AMP-activated protein kinase (AMPK) acts as a cellular fuel gauge, switching off ATP-consuming pathways and promoting alternative ATP generation in response to cellular stresses like ATP depletion.
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Fenofibrate activates AMPK and increases eNOS phosphorylation in HUVEC.
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Citations
Randomised, multicentre, placebo-controlled trial of fenofibrate for treatment of diabetic macular oedema with economic evaluation (FORTE study): study protocol for a randomised control trial
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Fenofibrate as an Adjunct Therapy for Ulcerative Colitis: Targeting Inflammation via SIRT1, NLRP3, and AMPK Pathways: A Randomized Controlled Pilot Study
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Fenofibrate Ameliorates Retinal Pigment Epithelium Injury Induced by Excessive Fat Through Upregulation of PI3K/AKT Signaling
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Perilipin 2–positive mononuclear phagocytes accumulate in the diabetic retina and promote PPARγ-dependent vasodegeneration
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