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Cited by 95PI3K/AKT/mTOR signaling in cancerMetabolism, Diabetes, and CancerAutophagy in Disease and Therapy

Mammalian target of rapamycin signaling in diabetic cardiovascular disease

Open access
Chong, Zhao, Maiese, Kenneth·2012·Cardiovascular Diabetology
DOI 10.1186/1475-2840-11-45PMC PMC3398846
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Abstract

Diabetes mellitus currently affects more than 170 million individuals worldwide and is expected to afflict another 200 million individuals in the next 30 years. Complications of diabetes as a result of oxidant stress affect multiple systems throughout the body, but involvement of the cardiovascular system may be one of the most severe in light of the impact upon cardiac and vascular function that can result in rapid morbidity and mortality for individuals. Given these concerns, the signaling pathways of the mammalian target of rapamycin (mTOR) offer exciting prospects for the development of novel therapies for the cardiovascular complications of diabetes. In the cardiovascular and metabolic systems, mTOR and its multi-protein complexes of TORC1 and TORC2 regulate insulin release and signaling, endothelial cell survival and growth, cardiomyocyte proliferation, resistance to β-cell injury, and cell longevity. Yet, mTOR can, at times, alter insulin signaling and lead to insulin resistance in the cardiovascular system during diabetes mellitus. It is therefore vital to understand the complex relationship mTOR and its downstream pathways hold during metabolic disease in order to develop novel strategies for the complications of diabetes mellitus in the cardiovascular system.

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  • The TSC1/TSC2 complex is a negative regulator of mTORC1 by controlling the activity of Rheb.

    “The TSC1/TSC2 complex is a negative regulator of mTORC1 by controlling the activity of Ras homologue enriched in brain (Rheb).”

    From Tuberous Sclerosis Protein 2 (TSC2) Modulates CCN4 Cytoprotection During Apoptotic Amyloid Toxicity in Microglia (2013) · cites this paper as [24]

    The section “mTOR signaling in diabetic cardiovascular disease” mentions TSC1/TSC2 in relation to IRS1 inhibition, not regulation of Rheb. A reference title links Rheb to increased mTORC1 signaling, but no passage found states that TSC1/TSC2 negatively regulates mTORC1 by controlling Rheb (searched: TSC1/TSC2, Rheb, and tuberous sclerosis complex). Page numbers were unavailable in our copy. (LLM, conf=0.73)

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Cited by

Sorted by citations

Authors
Chong, Z., & Maiese, K.
Corresponding author
Maiese, Kenneth
ORCID
Maiese, Kenneth
Venue
Cardiovascular Diabetology
Publisher
Springer Science and Business Media LLC
Published
2012
Volume
11
Issue
1
Pages
45
ISSN
1475-2840 (ISSN-L)
DOI
10.1186/1475-2840-11-45
PMC
PMC3398846
OpenAlex
W2145902922
Cited by
95
References
8
Citations by year
2024: 2 · 2023: 8 · 2022: 6 · 2021: 6 · 2020: 9 · 2019: 4 · 2018: 6 · 2017: 11 · 2016: 8 · 2015: 13 · 2014: 7 · 2013: 6 · 2012: 9
FWCI
1.02
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Cardiovascular Diabetology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • American Diabetes Association
  • American Heart Association
  • National Institutes of Health
  • National Institute on Aging
  • National Institute of Neurological Disorders and Stroke
  • National Institute of Environmental Health Sciences
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mTOR signaling, diabetic cardiovascular disease, diabetes mellitus, insulin resistance, TORC1, TORC2, insulin signaling, endothelial cell survival, cardiomyocyte proliferation, beta-cell injury, oxidative stress, cardiovascular complications of diabetes
MeSH terms
Animals, Cardiovascular Agents, Cardiovascular Diseases, Cardiovascular System, Diabetes Mellitus, Humans, Signal Transduction, Diabetes Complications, TOR Serine-Threonine Kinases

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