Evidence map›Paper›PMID 33599151›Full record

ReviewPhysiological reviews2021

Regulation and metabolic functions of mTORC1 and mTORC2.

Angelia Szwed, Eugene Kim, Estela Jacinto

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 505 papers.

0numbers the graph read from it
0cells of the map it votes in
505citing papers in PubMed
40.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

505 citing papers in PubMed, 735 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. mTORC2-NaChannels (Austin, Tex.) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Iron dysregulation in the central nervous system: implications for autism spectrum disorder.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  10. Glycolysis Drives TLR Ligand-Induced Maturation and Immune Activation of Liver Sinusoidal Endothelial Cells.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  11. Review
  12. The role of mTORC2/RICTOR in immune cells and inflammatory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Excess glutamine rewires endothelial cell metabolism.Metabolomics : Official journal of the Metabolomic Society · 2026
    Article
  20. Article

445 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Angelia SzwedDepartment of Biochemistry and Molecular Biology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, New Jersey.
Eugene KimDepartment of Biochemistry and Molecular Biology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, New Jersey.
Estela JacintoDepartment of Biochemistry and Molecular Biology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, New Jersey.ORCID 0000-0001-7118-1759
Rutgers, The State University of New Jersey · US

Funding

The Regulation of Cell Metabolism and Proliferation by mTOR complex 2R01GM079176 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI JACINTO, ESTELA · 2008 to 2017
$2.8M
The hexosamine biosynthesis pathway in metabolism and cell fateR01GM137493 · NIGMS · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI Estela Jacinto · 2020 to 2026
$2.6M
Cotranslational Functions of MTORR01CA154674 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI JACINTO, ESTELA · 2012 to 2017
$1.8M
NCI NIH HHS R01 CA154674NIGMS NIH HHS R01 GM079176NIGMS NIH HHS R01 GM137493
6 · The paper itself

Abstract

Cells metabolize nutrients for biosynthetic and bioenergetic needs to fuel growth and proliferation. The uptake of nutrients from the environment and their intracellular metabolism is a highly controlled process that involves cross talk between growth signaling and metabolic pathways. Despite constant fluctuations in nutrient availability and environmental signals, normal cells restore metabolic homeostasis to maintain cellular functions and prevent disease. A central signaling molecule that integrates growth with metabolism is the mechanistic target of rapamycin (mTOR). mTOR is a protein kinase that responds to levels of nutrients and growth signals. mTOR forms two protein complexes, mTORC1, which is sensitive to rapamycin, and mTORC2, which is not directly inhibited by this drug. Rapamycin has facilitated the discovery of the various functions of mTORC1 in metabolism. Genetic models that disrupt either mTORC1 or mTORC2 have expanded our knowledge of their cellular, tissue, as well as systemic functions in metabolism. Nevertheless, our knowledge of the regulation and functions of mTORC2, particularly in metabolism, has lagged behind. Since mTOR is an important target for cancer, aging, and other metabolism-related pathologies, understanding the distinct and overlapping regulation and functions of the two mTOR complexes is vital for the development of more effective therapeutic strategies. This review discusses the key discoveries and recent findings on the regulation and metabolic functions of the mTOR complexes. We highlight findings from cancer models but also discuss other examples of the mTOR-mediated metabolic reprogramming occurring in stem and immune cells, type 2 diabetes/obesity, neurodegenerative disorders, and aging.

Indexed as

AnimalsGlycolysisHumansLipid MetabolismMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Signal TransductionMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2cancer metabolismglycolysislipid metabolismmetabolic reprogrammingmTOR

Identifiers

PMID33599151
PMCPMC8424549
OpenAlexW3132255180

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.