Gene interactions and pathways from curated databases and text-mining
Science signaling 2009, PMID: 19293429

Obesity increases vascular senescence and susceptibility to ischemic injury through chronic activation of Akt and mTOR.

Wang, Chao-Yung; Kim, Hyung-Hwan; Hiroi, Yukio; Sawada, Naoki; Salomone, Salvatore; Benjamin, Laura E; Walsh, Kenneth; Moskowitz, Michael A; Liao, James K

Obesity and age are important risk factors for cardiovascular disease. However, the signaling mechanism linking obesity with age-related vascular senescence is unknown. Here we show that mice fed a high-fat diet show increased vascular senescence and vascular dysfunction compared to mice fed standard chow and are more prone to peripheral and cerebral ischemia. All of these changes involve long-term activation of the protein kinase Akt. In contrast, mice with diet-induced obesity that lack Akt1 are resistant to vascular senescence. Rapamycin treatment of diet-induced obese mice or of transgenic mice with long-term activation of endothelial Akt inhibits activation of mammalian target of rapamycin (mTOR)-rictor complex 2 and Akt, prevents vascular senescence without altering body weight, and reduces the severity of limb necrosis and ischemic stroke. These findings indicate that long-term activation of Akt-mTOR signaling links diet-induced obesity with vascular senescence and cardiovascular disease.

Diseases/Pathways annotated by Medline MESH: Cardiovascular Diseases, Disease Susceptibility, Ischemia, Obesity
Document information provided by NCBI PubMed

Text Mining Data

(mTOR)-rictor complex → Akt: " Rapamycin treatment of diet induced obese mice or of transgenic mice with long-term activation of endothelial Akt inhibits activation of mammalian target of rapamycin (mTOR)-rictor complex 2 and Akt, prevents vascular senescence without altering body weight, and reduces the severity of limb necrosis and ischemic stroke "

mammalian target of rapamycin (mTOR)-rictor → Akt: " Rapamycin treatment of diet induced obese mice or of transgenic mice with long-term activation of endothelial Akt inhibits activation of mammalian target of rapamycin (mTOR)-rictor complex 2 and Akt, prevents vascular senescence without altering body weight, and reduces the severity of limb necrosis and ischemic stroke "

Manually curated Databases

No curated data.