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Thus, signaling via mTOR may represent a novel mechanism whereby hypoxia augments mitogenstimulated vascular cell proliferation and angiogenesis.—Humar, R., Kiefer, F. N., Berns, H., Resink, T. J., Battegay, E. J. Hypoxia enhances vascular cell proliferation and angiogenesis in vitro via rapamycin (mTOR) ‐dependent signaling.
Akt signaling in the tumor vascular stroma was sensitive to rapamycin, suggesting that rapamycin may affect tumor growth in part by acting as a vascular Akt inhibitor.
Experimental data suggest that rapamycin may reduce angiogenesis and tumour growth by inhibiting the vascular endothelial growth factor (VEGF) pathway.
Rapamycin appears to inhibit tumor growth by halting tumor cell proliferation, inducing tumor cell apoptosis, and suppressing tumor angiogenesis.
Here we show that mammalian target of rapamycin (mTOR) signaling plays a key role in hypoxia‐triggered smooth muscle and endothelial proliferation and angiogenesis in vitro.
—Rapamycin potently inhibited early and mid stages of VEGF-A164–driven angiogenesis, but not late-stage angiogenesis or lymphangiogenesis.
Rapamycin combines antiproliferative and antiinflammatory properties and reduces neointima formation after angioplasty in patients.
Moreover, in vitro experiments showed that CsA promotes angiogenesis by a transforming growth factor-β–related mechanism, and that this effect is abrogated by rapamycin.
In conclusion, rapamycin suppresses angiogenesis and lymphangiogenesis in melanoma by blocking the mTOR signal pathway and subsequently downregulating the expression of VEGF-A/VEGFR-2 and VEGF-C/VEGFR-3.
According to our data rapamycin might have an anti-angiogenesis effect via inhibition of VEGF expression.

Related Questions

What is a background of using rapamycin in HCM cat(RAPACAT tria)?5 answersRapamycin has been studied in various contexts for its potential therapeutic effects. In a xenograft model of inclusion body myositis (IBM), rapamycin reduced the number of endomysial CD8+ T cells with 3-month treatment. In a rat myocardial infarction (MI)-induced chronic heart failure (HF) model, rapamycin improved cardiac function, inhibited cardiac remodeling, and reduced cardiomyocyte apoptosis while promoting autophagy. However, continuous rapamycin administration in lean mice led to the development of diabetes syndrome, inducing hyperglycemia and glucose intolerance. In preeclampsia-like mouse models, rapamycin improved clinical manifestations and blood lipid profiles. In patients with autosomal dominant polycystic kidney disease (ADPKD), rapamycin did not decrease kidney volume or cystic growth, but it did not significantly increase proteinuria or decrease estimated glomerular filtration rate (eGFR). The background of using rapamycin in hypertrophic cardiomyopathy (HCM) cats (RAPACAT trial) was not mentioned in the provided abstracts.
Does lifelong rapamycin administration increase lifespan in mice?5 answersLifelong administration of rapamycin has been shown to increase lifespan in mice. This finding has led to increased interest in studying the effects of rapamycin on aging and age-related diseases in mice. Rapamycin has been found to improve health during aging and demonstrate efficacy when started later in life. It has been shown to improve physical function and cardiac structure in aged mice, regardless of the age at which treatment is started. Furthermore, rapamycin treatment has been associated with a significant improvement in survival in both male and female mice with germline PTEN loss, a mouse model of cancer predisposition. These findings suggest that rapamycin may have potential as a treatment for age-related diseases and cancer prevention in both germline cancer predisposition and sporadic cancers with genetic PI3K pathway activation.
Does Mtor stimulate angiogenesis?10 answers
Does VEGF stimulate angiogenesis?10 answers
Does angiogenesis inhibit tumor growth?10 answers
How do you speed up angiogenesis?9 answers

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