Evidence map›Paper›PMID 34830375›Full record

ReviewInternational journal of molecular sciences2021

Melatonin and Pathological Cell Interactions: Mitochondrial Glucose Processing in Cancer Cells.

Russel J Reiter, Ramaswamy Sharma, Sergio Rosales-Corral, Walter Manucha, Luiz Gustavo de Almeida Chuffa, Debora Aparecida Pires de Campos Zuccari

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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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.

Russel J ReiterDepartment of Cell Systems & Anatomy, Joe R. and Teresa Lozano Long School of Medicine, UT Health San Antonio, San Antonio, TX 78229, USA.ORCID 0000-0001-6763-4225
Ramaswamy SharmaDepartment of Cell Systems & Anatomy, Joe R. and Teresa Lozano Long School of Medicine, UT Health San Antonio, San Antonio, TX 78229, USA.ORCID 0000-0003-2346-5305
Sergio Rosales-CorralCentro de Investigacion Biomedica de Occidente, Instituto Mexicano del Seguro Social, Guadalajara 45150, Mexico.
Walter ManuchaInstituto de Medicina y Biologia Experimental de Cuyo (IMBECU), Consejo Nacional de Investigaciones Cientificas y Tecnologicas (CONICET), Mendoza 5500, Argentina.ORCID 0000-0002-2279-7626
Luiz Gustavo de Almeida ChuffaDepartment of Structural and Functional Biology, Institute of Biosciences of Botucatu, Botucatu 18618-689, Brazil.ORCID 0000-0002-0199-3396
Debora Aparecida Pires de Campos ZuccariLaboratorio de Investigacao Molecular do Cancer, Faculdade de Medicina de Sao Jose do Rio Preto, Sao Jose do Rio Preto 15080-000, Brazil.ORCID 0000-0002-0146-9041

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin is synthesized in the pineal gland at night. Since melatonin is produced in the mitochondria of all other cells in a non-circadian manner, the amount synthesized by the pineal gland is less than 5% of the total. Melatonin produced in mitochondria influences glucose metabolism in all cells. Many pathological cells adopt aerobic glycolysis (Warburg effect) in which pyruvate is excluded from the mitochondria and remains in the cytosol where it is metabolized to lactate. The entrance of pyruvate into the mitochondria of healthy cells allows it to be irreversibly decarboxylated by pyruvate dehydrogenase (PDH) to acetyl coenzyme A (acetyl-CoA). The exclusion of pyruvate from the mitochondria in pathological cells prevents the generation of acetyl-CoA from pyruvate. This is relevant to mitochondrial melatonin production, as acetyl-CoA is a required co-substrate/co-factor for melatonin synthesis. When PDH is inhibited during aerobic glycolysis or during intracellular hypoxia, the deficiency of acetyl-CoA likely prevents mitochondrial melatonin synthesis. When cells experiencing aerobic glycolysis or hypoxia with a diminished level of acetyl-CoA are supplemented with melatonin or receive it from another endogenous source (pineal-derived), pathological cells convert to a more normal phenotype and support the transport of pyruvate into the mitochondria, thereby re-establishing a healthier mitochondrial metabolic physiology.

Indexed as

AerobiosisCell CommunicationGlucoseGlycolysisHumansMelatoninMitochondriaNeoplasmsWarburg Effect, OncologicGlucoseMelatonin

Identifiers

PMID34830375
PMCPMC8621753

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Registered trials

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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.