Evidence map›Paper›PMID 32234503›Full record

ReviewProgress in lipid research2020

Regulation of coenzyme A levels by degradation: the 'Ins and Outs'.

Philippe Naquet, Evan W Kerr, Schuyler D Vickers, Roberta Leonardi

Open access · bronzeAbstract readReview
In one paragraph

Review in Progress in lipid research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 115 citations in OpenAlex.

  1. Expanding bile acid diversityNatural product reports · 2026
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  14. Dysregulated Fatty Acid Metabolism in Preeclampsia Among Highland Andeans: Insights Into Adaptive and Maladaptive Placental Metabolic Phenotypes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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9 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

4 authors at 2 institutions in 2 countries.

Philippe NaquetAix Marseille Univ, INSERM, CNRS, Centre d'Immunologie de Marseille-Luminy, Marseille, France. Electronic address: naquet@ciml.univ-mrs.fr.
Evan W KerrDepartment of Biochemistry, West Virginia University, Morgantown, West Virginia 26506, United States of America.
Schuyler D VickersDepartment of Biochemistry, West Virginia University, Morgantown, West Virginia 26506, United States of America.
Roberta LeonardiDepartment of Biochemistry, West Virginia University, Morgantown, West Virginia 26506, United States of America. Electronic address: roleonardi@hsc.wvu.edu.
West Virginia University · USCentre d’Immunologie de Marseille-Luminy · FR

Funding

Changes in Coenzyme A Levels are a Key Mechanism Regulating Metabolic PathwaysR35GM119528 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Roberta Leonardi · 2016 to 2026
$4.4M
The effect of mitochondrial CoA degradation on glucose and fatty acid metabolismF31DK118878 · NIDDK · WEST VIRGINIA UNIVERSITY · PI KERR, EVAN W · 2019 to 2020
$84k
NIDDK NIH HHS F31 DK118878NIGMS NIH HHS R35 GM119528
6 · The paper itself

Abstract

Coenzyme A (CoA) is the predominant acyl carrier in mammalian cells and a cofactor that plays a key role in energy and lipid metabolism. CoA and its thioesters (acyl-CoAs) regulate a multitude of metabolic processes at different levels: as substrates, allosteric modulators, and via post-translational modification of histones and other non-histone proteins. Evidence is emerging that synthesis and degradation of CoA are regulated in a manner that enables metabolic flexibility in different subcellular compartments. Degradation of CoA occurs through distinct intra- and extracellular pathways that rely on the activity of specific hydrolases. The pantetheinase enzymes specifically hydrolyze pantetheine to cysteamine and pantothenate, the last step in the extracellular degradation pathway for CoA. This reaction releases pantothenate in the bloodstream, making this CoA precursor available for cellular uptake and de novo CoA synthesis. Intracellular degradation of CoA depends on specific mitochondrial and peroxisomal Nudix hydrolases. These enzymes are also active against a subset of acyl-CoAs and play a key role in the regulation of subcellular (acyl-)CoA pools and CoA-dependent metabolic reactions. The evidence currently available indicates that the extracellular and intracellular (acyl-)CoA degradation pathways are regulated in a coordinated and opposite manner by the nutritional state and maximize the changes in the total intracellular CoA levels that support the metabolic switch between fed and fasted states in organs like the liver. The objective of this review is to update the contribution of these pathways to the regulation of metabolism, physiology and pathology and to highlight the many questions that remain open.

Indexed as

ProteolysisAnimalsCoenzyme AHumansCoenzyme ACoenzyme AMetabolic regulationNudix hydrolasePantetheinasesPantothenate/organelles

Identifiers

PMID32234503
PMCPMC7234920
OpenAlexW3013570983

What OpenQuestion holds

Textmetadata
LicenceTDM
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.