Evidence map›Paper›PMID 30386301›Full record

ReviewFrontiers in endocrinology2018

mTORC1 Overactivation as a Key Aging Factor in the Progression to Type 2 Diabetes Mellitus.

Carlos Guillén, Manuel Benito

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
9.0field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 80 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
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  9. Article
  10. Inflammaging and Brain Aging.International journal of molecular sciences · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Inhalation exposure-induced toxicity and disease mediated via mTOR dysregulation.Experimental biology and medicine (Maywood, N.J.) · 2024
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Ageing in the brain: mechanisms and rejuvenating strategies.Cellular and molecular life sciences : CMLS · 2023
    Review
  20. Article
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

2 authors at 2 institutions in 1 country.

Carlos GuillénDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Manuel BenitoDepartment of Biochemistry and Molecular Biology, Faculty of Pharmacy, Complutense University of Madrid, Madrid, Spain.
Centro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESSpanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 Diabetes Mellitus (T2DM), a worldwide epidemics, is a progressive disease initially developing an insulin resistant state, with manifest pancreatic beta islet overwork and hyperinsulinemia. As the disease progresses, pancreatic β cells are overwhelmed and fails in their capacity to compensate insulin resistance. In addition, it is usually associated with other metabolic diseases such as hyperlipidemia, obesity and the metabolic syndrome. During the progression to T2DM there is a chronic activation of mTORC1 signaling pathway, which induces aging and acts as an endogenous inhibitor of autophagy. The complex 1 of mTOR (mTORC1) controls cell proliferation, cell growth as well as metabolism in a variety of cell types through a complex signaling network. Autophagy is involved in the recycling of cellular components for energy generation under nutrient deprivation, and serves as a complementary degradation system to the ubiquitin-proteasome pathway. Autophagy represents a protective mechanism for different cell types, including pancreatic β cells, and potentiates β cell survival across the progression to T2DM. Here, we focus our attention on the chronic overactivation of mTORC1 signaling pathway in β islets from prediabetics patients, making these cells more prone to trigger apoptosis upon several cellular stressors and allowing the progression from prediabetes to type 2 diabetes status.

Indexed as

amylinautophagymitophagymTORC1T2DMTSC2

Identifiers

PMID30386301
PMCPMC6198057
OpenAlexW2897782627

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.