Evidence map›Paper›PMID 26378592›Full record

ReviewBiomolecules2015

The Impact of Non-Enzymatic Reactions and Enzyme Promiscuity on Cellular Metabolism during (Oxidative) Stress Conditions.

Gabriel Piedrafita, Markus A Keller, Markus Ralser

Abstract readReview
In one paragraph

Review in Biomolecules, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. An atlas of ferroptosis-induced secretomes.Cell death and differentiation · 2025
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. SARS- CoV-2 infection and oxidative stress in early-onset preeclampsia.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Review
  13. Article
  14. Molecular Damage in Aging.Nature aging · 2021
    Review
  15. Article
  16. Article
  17. Are insulin-resistance and oxidative stress cause or consequence of aging.Experimental biology and medicine (Maywood, N.J.) · 2020
    Article
  18. Article
  19. Article
  20. Review
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.

Gabriel PiedrafitaDepartment of Biochemistry, University of Cambridge, 80 Tennis Court Rd, Cambridge CB2 1GA, UK. gp394@cam.ac.uk.
Markus A KellerDepartment of Biochemistry, University of Cambridge, 80 Tennis Court Rd, Cambridge CB2 1GA, UK. mk747@cam.ac.uk.
Markus RalserDepartment of Biochemistry, University of Cambridge, 80 Tennis Court Rd, Cambridge CB2 1GA, UK. markus.ralser@crick.ac.uk.

Funding

Wellcome Trust RG 093735/Z/10/Z
6 · The paper itself

Abstract

Cellular metabolism assembles in a structurally highly conserved, but functionally dynamic system, known as the metabolic network. This network involves highly active, enzyme-catalyzed metabolic pathways that provide the building blocks for cell growth. In parallel, however, chemical reactivity of metabolites and unspecific enzyme function give rise to a number of side products that are not part of canonical metabolic pathways. It is increasingly acknowledged that these molecules are important for the evolution of metabolism, affect metabolic efficiency, and that they play a potential role in human disease-age-related disorders and cancer in particular. In this review we discuss the impact of oxidative and other cellular stressors on the formation of metabolic side products, which originate as a consequence of: (i) chemical reactivity or modification of regular metabolites; (ii) through modifications in substrate specificity of damaged enzymes; and (iii) through altered metabolic flux that protects cells in stress conditions. In particular, oxidative and heat stress conditions are causative of metabolite and enzymatic damage and thus promote the non-canonical metabolic activity of the cells through an increased repertoire of side products. On the basis of selected examples, we discuss the consequences of non-canonical metabolic reactivity on evolution, function and repair of the metabolic network.

Indexed as

Metabolic Networks and PathwaysOxidative StressBiological EvolutionHumansOxidation-ReductionSubstrate Specificityenzyme promiscuitymetabolic damagemetabolite repairoxidative stressreactive oxygen speciesunderground metabolism

Identifiers

PMID26378592
PMCPMC4598790

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.