Evidence map›Paper›PMID 34277603›Full record

ReviewFrontiers in cell and developmental biology2021

The mTOR-Autophagy Axis and the Control of Metabolism.

Nerea Deleyto-Seldas, Alejo Efeyan

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07175051 (Targeting the Pathophysiology of Sickle Cell-Related Kidney Disease Using the SGLT2 Inhibitors, Empagliflozin), which is not on this map. Cited by 204 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
204citing papers in PubMed, 2 pooled it
30.3field-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.

NCT07175051 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

Targeting the Pathophysiology of Sickle Cell-Related Kidney Disease Using the SGLT2 Inhibitors, Empagliflozin

TypeinterventionalSponsorUniversity of Illinois at ChicagoRan2026 to 2030Enrolled20ConditionsSickle Cell Anemia (HbSS, or HbSβ-thalassemia0), AlbuminuriaArmsEmpagliflozin (oral)
3 · Its place in the literature

Who cites it

204 citing papers in PubMed, 2 syntheses or guidelines pooled it, 313 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Review
  7. Review
  8. Role of Autophagy in Scleral Remodeling During Form-Deprivation Myopia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  9. Article
  10. CCDC137 affects sorafenib resistance in hepatocellular carcinoma cells by activating the AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  11. Article
  12. Crosstalk between autophagy and ferroptosis in liver diseases (Review).International journal of molecular medicine · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

144 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

2 authors at 2 institutions in 1 country.

Nerea Deleyto-SeldasMetabolism and Cell Signaling Laboratory, Spanish National Cancer Research Center (CNIO), Madrid, Spain.
Alejo EfeyanMetabolism and Cell Signaling Laboratory, Spanish National Cancer Research Center (CNIO), Madrid, Spain.
Centro de Investigación del Cáncer · ESSpanish National Cancer Research Centre · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanistic target of rapamycin (mTOR), master regulator of cellular metabolism, exists in two distinct complexes: mTOR complex 1 and mTOR complex 2 (mTORC1 and 2). MTORC1 is a master switch for most energetically onerous processes in the cell, driving cell growth and building cellular biomass in instances of nutrient sufficiency, and conversely, allowing autophagic recycling of cellular components upon nutrient limitation. The means by which the mTOR kinase blocks autophagy include direct inhibition of the early steps of the process, and the control of the lysosomal degradative capacity of the cell by inhibiting the transactivation of genes encoding structural, regulatory, and catalytic factors. Upon inhibition of mTOR, autophagic recycling of cellular components results in the reactivation of mTORC1; thus, autophagy lies both downstream and upstream of mTOR. The functional relationship between the mTOR pathway and autophagy involves complex regulatory loops that are significantly deciphered at the cellular level, but incompletely understood at the physiological level. Nevertheless, genetic evidence stemming from the use of engineered strains of mice has provided significant insight into the overlapping and complementary metabolic effects that physiological autophagy and the control of mTOR activity exert during fasting and nutrient overload.

Indexed as

autophagylysosomemechanistic target of rapamycinmetabolismnutrients

Identifiers

PMID34277603
PMCPMC8281972
OpenAlexW3185746211

What OpenQuestion holds

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Registered trials

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.