Does Mtor stimulate angiogenesis?
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364 Citations | 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. |
| Our studies suggest that mTOR regulates vascular integrity and function and that mTOR attenuation may restore neurovascular function and cardiovascular health. | |
Open access•Journal Article 28 Citations | Taken together, these data revealed that mTOR signaling pathway regulates tumor angiogenesis by EGFR/p-Stat3(T705) and HIF-1α/PAI. |
26 Citations | Taken together, these results indicate that mTOR signaling is involved in visfatin-induced angiogenesis, and that this signaling leads to visfatin-induced VEGF expression and nuclear translocation of β-catenin. |
139 Citations | Although often called ‘a master regulator,’ mTOR is but one signal in an intricate signaling cascade that controls cell growth and angiogenesis in both normal and cancerous conditions. |
01 Jan 2016 4 Citations | mTOR appears to act as the molecular link between metabolite status of the cell and angiogenesis by integrating metabolite-sensing mechanisms to modulate the expression of angiogenic factors. |
| These observations suggest that mTOR is likely to be involved in sensing membrane sterol concentrations in endothelial cells, and the cholesterol trafficking pathway is a promising target for the discovery of inhibitors of angiogenesis. | |
| The mTOR pathway modulates the interactions between the stroma and the tumor, thereby affecting both the tumor immunity and angiogenesis. | |
10 Citations | The present study thus provides mechanistic evidence to the previously reported multifaceted anti-angiogenic effects of PA. Our study further identified mTOR signaling as an important target of PA, and therefore highlights the potential of PA for therapeutic intervention against angiogenesis-related pathogenesis, particularly, metastatic malignancy. |
| Our work explains why human cancers with aberrant mTOR signaling are prone to angiogenesis and suggests that inhibition of mTOR with rapamycin might be a suitable therapeutic strategy. |
Related Questions
What is the role of mTOR in adipose tissue?4 answersmTOR plays a crucial role in regulating adipose tissue function, including adipogenesis, lipid metabolism, thermogenesis, and adipokine synthesis and/or secretion. It is involved in the crosstalk between liver and adipose tissue in the pathogenesis of alcohol-associated liver disease (ALD). Adipocyte-specific deletion of mTOR leads to hepatomegaly, adipose tissue atrophy, and increased liver injury and inflammation in response to alcohol. mTOR also regulates energy metabolism and cell growth in adipose tissue, and its deletion in adipocytes causes reduction of brown adipose tissue (BAT) and inguinal white adipose tissue (iWAT) mass. Additionally, mTOR is involved in the regulation of adipose tissue browning, where white adipose tissue acquires thermogenic metabolism in response to cold challenge. Loss of mTORC1 activity leads to increased browning of white adipose tissue, while its hyperactivation inhibits browning at thermoneutrality. These findings highlight the critical role of mTOR in adipose tissue biology and its potential as a pharmacological target for obesity and metabolic diseases.
LIMITATION OF temsirolimus mTOR pathway?3 answersThe limitation of temsirolimus in targeting the mTOR pathway is its limited antitumor activity in clinical contexts, even when combined with other drugs. Rapamycin and its derivatives, known as rapalogs, have shown limited effectiveness in most clinical trials, leading to the development of novel mTOR inhibitors with stronger antineoplastic potency. However, emerging clinical data suggest that these novel mTOR-targeting drugs may also have weak antitumor activity. Despite the potential of mTOR as a therapeutic target for cancer treatment, the efficacy of mTOR inhibitors remains a challenge.
What exact research can be conducted around the relationship between mtor and dip2a?5 answersStep 1: Answer without citation
Research can be conducted to further explore the role of mTOR signaling in the pathophysiology of anxiety and other psychiatric disorders, particularly in relation to Dip2a. Additionally, investigating the potential therapeutic implications of targeting mTOR signaling in conditions such as autism and anxiety, as well as in multiple myeloma, could provide valuable insights for the development of novel treatment strategies. Furthermore, understanding the molecular mechanisms underlying the interaction between mTOR and Dip2a, and its impact on dendritic morphology and neuronal function, could offer new avenues for addressing neurodevelopmental and psychiatric conditions.
Step 3: Answer with citation
Research can be conducted to further explore the role of mTOR signaling in the pathophysiology of anxiety and other psychiatric disorders, particularly in relation to Dip2a. Additionally, investigating the potential therapeutic implications of targeting mTOR signaling in conditions such as autism and anxiety, as well as in multiple myeloma, could provide valuable insights for the development of novel treatment strategies. Furthermore, understanding the molecular mechanisms underlying the interaction between mTOR and Dip2a, and its impact on dendritic morphology and neuronal function, could offer new avenues for addressing neurodevelopmental and psychiatric conditions.
Which transcription factors are regulated by mTOR?5 answersmTOR regulates multiple cellular processes and is involved in the transcriptional regulation of various transcription factors. The transcription factors HAND and MYOD are recognized by the conserved motifs AGGCGGG and GGCGGC, respectively, in the promoter region of mTOR. Additionally, the FoxO3a transcription factor is coordinately regulated by mTORC1 and mTORC2, and plays a crucial role in controlling cell proliferation. The transcription factor MZF1 binds to the cis-element TGGGGA in the Mtor promoter region and down-regulates Mtor expression. These findings suggest that HAND, MYOD, FoxO3a, and MZF1 are transcription factors that are regulated by mTOR.
What are the effects of mutations in mTOR localization on cell growth?5 answersMutations in mTOR localization have been shown to have effects on cell growth. Activating mutations in mTOR enhance growth in a cell type agnostic manner under nutrient-replete conditions, but are detrimental to cell survival in nutrient-poor conditions. Additionally, oncogenic mutations in the nutrient-sensing arm of the mTOR pathway display a similar phenotype and are rare in human cancers of all types. Loss of the mTOR pathway negative regulator PTEN from hippocampal dentate granule cells leads to neuronal hypertrophy and aberrant basal dendrite formation. Mutations in mTOR pathway genes can cause brain overgrowth and intellectual disability, with the mTOR activator gene RHEB associated with megalencephaly when mutated. These findings suggest that mutations in mTOR localization can have significant effects on cell growth and brain development.
What are the different mechanisms of mTOR activation and inhibition?4 answersL'activation de mTOR est régulée par la petite GTPase RHEB, qui se lie à mTOR et provoque un changement de conformation qui accélère la catalyse. Des mutations hyperactivantes dans les éléments structuraux associés au mTOR peuvent imiter le RHEB et atténuer l'auto-inhibition, entraînant l'activation du mTOR. mTORC1 sélectionne également ses substrats grâce à la reconnaissance du motif de la séquence de signalisation Tor (TOS) par la sous-unité RAPTOR. L'inhibition de mTORC1 est médiée par le PRAS40, qui inhibe le recrutement du substrat vers mTORC1. La liaison de la rapamycine à la mTOR peut également inhiber l'activité de la mTOR en bloquant le recrutement du substrat. Dans les tumeurs stromales gastro-intestinales (GIST), l'activation de la voie PI3K/mTOR peut se produire par le biais de mutations liées au gain de fonction dans le KIT ou de mutations dans le PIK3CA ou le PTEN, entraînant l'activation de mTOR. Dans la maladie d'Alzheimer, l'activation chronique de mTOR est impliquée dans le dysfonctionnement métabolique et la progression de la maladie, et l'inhibition du SGLT2 peut rétablir le cycle mTOR et potentiellement diminuer la progression de la maladie d'Alzheimer.