Evidence map›Paper›PMID 33852870›Full record

ArticleCell reports2021

A naturally occurring mutation in ATP synthase subunit c is associated with increased damage following hypoxia/reoxygenation in STEMI patients.

Giampaolo Morciano, Gaia Pedriali, Massimo Bonora, Rita Pavasini, Elisa Mikus, Simone Calvi, Matteo Bovolenta, Magdalena Lebiedzinska-Arciszewska, Mirko Pinotti, Alberto Albertini and 6 more

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Cell reports, 2021. 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
2.3field-weighted citation impact, top 11% 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, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 6 institutions in 5 countries.

Giampaolo MorcianoMaria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy; Department of Medical Sciences, Section of Experimental Medicine, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Gaia PedrialiMaria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy.
Massimo BonoraDepartment of Medical Sciences, Section of Experimental Medicine, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Rita PavasiniCardiovascular Institute, Azienda Ospedaliero-Universitaria di Ferrara, Cona, 44121 Ferrara, Italy.
Elisa MikusCardiothoracic and Vascular Department, Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy.
Simone CalviCardiothoracic and Vascular Department, Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy.
Matteo BovolentaGenethon, INSERM UMR951, 1 bis, rue de l'Internationale BP60, 91002 Evry Cedex, France.
Magdalena Lebiedzinska-ArciszewskaLaboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Mirko PinottiDepartment of Life Sciences and Biotechnology, University of Ferrara, 44121 Ferrara, Italy.
Alberto AlbertiniCardiothoracic and Vascular Department, Maria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy.
Mariusz R WieckowskiLaboratory of Mitochondrial Biology and Metabolism, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
Carlotta GiorgiDepartment of Medical Sciences, Section of Experimental Medicine, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy.
Roberto FerrariMaria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy; Cardiovascular Institute, Azienda Ospedaliero-Universitaria di Ferrara, Cona, 44121 Ferrara, Italy.
Lorenzo GalluzziDepartment of Radiation Oncology, Weill Cornell Medical College, New York, NY, USA; Sandra and Edward Meyer Cancer Center, New York, NY, USA; Caryl and Israel Englander Institute for Precision Medicine, New York, NY, USA; Department of Dermatology, Yale School of Medicine, New Haven, CT, USA; Université de Paris, Paris, France.
Gianluca CampoMaria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy; Cardiovascular Institute, Azienda Ospedaliero-Universitaria di Ferrara, Cona, 44121 Ferrara, Italy.
Paolo PintonMaria Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy; Department of Medical Sciences, Section of Experimental Medicine, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, 44121 Ferrara, Italy. Electronic address: paolo.pinton@unife.it.
Maria Cecilia Hospital · ITUniversity of Ferrara · ITInstytut Biologii Doświadczalnej im. Marcelego Nenckiego · PLArcispedale Sant'Anna · ITInserm · FRUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Preclinical models of ischemia/reperfusion injury (RI) demonstrate the deleterious effects of permeability transition pore complex (PTPC) opening in the first minutes upon revascularization of the occluded vessel. The ATP synthase c subunit (Csub) influences PTPC activity in cells, thus impacting tissue injury. A conserved glycine-rich domain in Csub is classified as critical because, when mutated, it modifies ATP synthase properties, protein interaction with the mitochondrial calcium (Ca

Indexed as

AgedAnimalsBase SequenceCalcium ChannelsExonsFemaleGene ExpressionHumansHypoxiaIntronsMaleMiddle AgedMitochondriaMitochondrial Permeability Transition PoreMitochondrial Proton-Translocating ATPasesMutationATP5F1A protein, humanATP5MC1 protein, humanCalcium Channelsmitochondrial calcium uniporterMitochondrial Permeability Transition PoreMitochondrial Proton-Translocating ATPasesOxygenATP synthasecardiovascular diseasesglycine-rich domainischemiamitochondriaPTPreperfusion injurySTEMI patientssubunit c

Identifiers

PMID33852870
OpenAlexW3154822189

What OpenQuestion holds

Textmetadata
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.