Evidence map›Paper›PMID 32527005›Full record

ArticleJournal of clinical medicine2020

Mitochondrial Energetics and Ca2

Maria Lombardi, Davide Lazzeroni, Annalinda Pisano, Francesca Girolami, Ottavio Alfieri, Giovanni La Canna, Giulia d'Amati, Iacopo Olivotto, Ornella E Rimoldi, Chiara Foglieni and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Mitochondrial Dysfunction in Cardiac Surgery.Anesthesiology clinics · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Article
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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

11 authors at 5 institutions in 1 country.

Maria LombardiCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
Davide LazzeroniCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
Annalinda PisanoDepartment of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome and Policlinico Umberto I, 00161 Rome, Italy.
Francesca GirolamiCardiology Unit, Meyer Children's Hospital, 50139 Florence, Italy.
Ottavio AlfieriCardiac Surgery Unit, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
Giovanni La CannaApplied Diagnostic Echocardiography Unit, Cardiovascular Department, Humanitas Clinical and Research Hospital, 20089 Rozzano-Milan, Italy.
Giulia d'AmatiDepartment of Radiological, Oncological and Pathological Sciences, Sapienza University of Rome and Policlinico Umberto I, 00161 Rome, Italy.ORCID 0000-0002-6959-691X
Iacopo OlivottoCardiomyopathy Unit, Careggi University Hospital, 50139 Florence, Italy.
Ornella E RimoldiInstitute of Molecular Bioimaging and Physiology, National Research Council (IBFM-CNR), 20090 Segrate-Milan, Italy.
Chiara FoglieniCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
Paolo G CamiciCardiovascular Research Center, IRCCS San Raffaele Scientific Institute, 20132 Milan, Italy.
Vita-Salute San Raffaele University · ITPoliclinico Umberto I · ITAzienda Ospedaliero-Universitaria Careggi · ITInstitute of Molecular Bioimaging and Physiology · ITMeyer Children's Hospital · IT

Funding

Ministero della Salute NET-2011-02347173
6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is the most common genetic disease of the myocardium associated to mutations in sarcomeric genes, but the link between genotype and phenotype remains poorly understood. Magnetic resonance spectroscopy studies have demonstrated impaired cardiac energetics in patients with HCM, and altered mitochondria were described in biopsies, but little is known about possible perturbations of mitochondrial function and adenosine triphosphate (ATP) production/consumption. The aim of this study was to investigate possible abnormalities in mitochondrial enzymes generating/scavenging reactive oxygen species, and changes in the Ca

Indexed as

Ca2+-activated ATPasemitochondrial Complex I (NADH dehydrogenase)mitochondrial Complex V (ATP synthase)mitochondrial energeticsobstructive hypertrophic cardiomyopathy (HCM)reactive oxygen species (ROS) scavenger enzymes

Identifiers

PMID32527005
PMCPMC7356244
OpenAlexW3035364805

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.