Evidence map›Paper›PMID 28546851›Full record

ReviewOxidative medicine and cellular longevity2017

Monoamine Oxidases, Oxidative Stress, and Altered Mitochondrial Dynamics in Cardiac Ageing.

Damien Maggiorani, Nicola Manzella, Dale E Edmondson, Andrea Mattevi, Angelo Parini, Claudia Binda, Jeanne Mialet-Perez

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.4field-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

57 citing papers in PubMed, 109 citations in OpenAlex.

  1. Prenylcysteine Oxidase 1 Deficiency Protects the Cardiac Muscle Cell Line HL-1 Against Ischaemic/Hypoxic Stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  10. Synthesis of 1,2,4-Oxadiazin-5(6Molecules (Basel, Switzerland) · 2024
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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

7 authors at 3 institutions in 3 countries.

Damien MaggioraniInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM, Université de Toulouse, Toulouse, France.
Nicola ManzellaInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM, Université de Toulouse, Toulouse, France.
Dale E EdmondsonDepartment of Biochemistry, Emory University School of Medicine, 1510 Clifton Road, Atlanta, GA, USA.
Andrea MatteviDepartment of Biology and Biotechnology, University of Pavia, Via Ferrata 1, 27100 Pavia, Italy.
Angelo PariniInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM, Université de Toulouse, Toulouse, France.
Claudia BindaDepartment of Biology and Biotechnology, University of Pavia, Via Ferrata 1, 27100 Pavia, Italy.
Jeanne Mialet-PerezInstitut des Maladies Métaboliques et Cardiovasculaires, INSERM, Université de Toulouse, Toulouse, France.ORCID 0000-0002-1765-0283
Inserm · FRUniversity of Pavia · ITEmory University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The advances in healthcare over the past several decades have resulted in populations now living longer. With this increase in longevity, a wider prevalence of cardiovascular diseases is more common and known to be a major factor in rising healthcare costs. A wealth of scientific evidence has implicated cell senescence as an important component in the etiology of these age-dependent pathologies. A number of studies indicate that an excess of reactive oxygen species (ROS) contributes to trigger and accelerate the cardiac senescence processes, and a new role of monoamine oxidases, MAO-A and MAO-B, is emerging in this context. These mitochondrial enzymes regulate the level of catecholamines and serotonin by catalyzing their oxidative deamination in the heart. MAOs' expression substantially increases with ageing (6-fold MAO-A in the heart and 4-fold MAO-B in neuronal tissue), and their involvement in cardiac diseases is supposedly related to the formation of ROS, via the hydrogen peroxide produced during the substrate degradation. Here, we will review the most recent advances in this field and describe why MAOs could be effective targets in order to prevent age-associated cardiovascular disease.

Indexed as

Mitochondrial DynamicsOxidative StressAgingAnimalsHeartHumansMonoamine OxidaseReactive Oxygen SpeciesMonoamine OxidaseReactive Oxygen Species

Identifiers

PMID28546851
PMCPMC5435992
OpenAlexW2610683753

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.