Evidence map›Paper›PMID 35325070›Full record

ReviewCardiovascular research2023

The regulation of cardiac intermediary metabolism by NADPH oxidases.

Adam A Nabeebaccus, Christina M Reumiller, Jie Shen, Anna Zoccarato, Celio X C Santos, Ajay M Shah

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  4. Article
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  8. Article
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  10. Review
  11. Immunometabolism in the Aging Heart.Journal of the American Heart Association · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Progress of nanomaterials in the treatment of thrombus.Drug delivery and translational research · 2024
    Review
  19. 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

6 authors at 1 institution in 1 country.

Adam A NabeebaccusSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.ORCID 0000-0002-1600-1492
Christina M ReumillerSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Jie ShenSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.ORCID 0000-0002-5339-5638
Anna ZoccaratoSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Celio X C SantosSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.
Ajay M ShahSchool of Cardiovascular Medicine and Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London SE5 9NU, UK.ORCID 0000-0002-6547-0631
King's College London · GB

Funding

British Heart Foundation CH/1999001/11735British Heart Foundation RE/18/2/34213British Heart Foundation RG/13/11/30384British Heart Foundation RG/20/3/34823
6 · The paper itself

Abstract

NADPH oxidases (NOXs), enzymes whose primary function is to generate reactive oxygen species, are important regulators of the heart's physiological function and response to pathological insults. The role of NOX-driven redox signalling in pathophysiological myocardial remodelling, including processes such as interstitial fibrosis, contractile dysfunction, cellular hypertrophy, and cell survival, is well recognized. While the NOX2 isoform promotes many detrimental effects, the NOX4 isoform has attracted considerable attention as a driver of adaptive stress responses both during pathology and under physiological states such as exercise. Recent studies have begun to define some of the NOX4-modulated mechanisms that may underlie these adaptive responses. In particular, novel functions of NOX4 in driving cellular metabolic changes have emerged. Alterations in cellular metabolism are a recognized hallmark of the heart's response to physiological and pathological stresses. In this review, we highlight the emerging roles of NOX enzymes as important modulators of cellular intermediary metabolism in the heart, linking stress responses not only to myocardial energetics but also other functions. The novel interplay of NOX-modulated redox signalling pathways and intermediary metabolism in the heart is unravelling a new aspect of the fascinating biology of these enzymes which will inform a better understanding of how they drive adaptive responses. We also discuss the implications of these new findings for therapeutic approaches that target metabolism in cardiac disease.

Indexed as

MyocardiumNADPH OxidasesHeartNADPH Oxidase 4Oxidative StressProtein IsoformsReactive Oxygen SpeciesNADPH Oxidase 4NADPH OxidasesProtein IsoformsReactive Oxygen SpeciesCardiac metabolismIntermediary metabolismNADPH oxidasesRedox signalling

Identifiers

PMID35325070
PMCPMC9847558
OpenAlexW4220984077

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.