Evidence map›Paper›PMID 31049138›Full record

ArticleOxidative medicine and cellular longevity2019

New Insights into the Hepcidin-Ferroportin Axis and Iron Homeostasis in iPSC-Derived Cardiomyocytes from Friedreich's Ataxia Patient.

Alessandra Bolotta, Provvidenza Maria Abruzzo, Vito Antonio Baldassarro, Alessandro Ghezzo, Katia Scotlandi, Marina Marini, Cinzia Zucchini

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Epigenetic regulation of ferroptosis in gastrointestinal cancers (Review).International journal of molecular medicine · 2025
    Review
  3. Review
  4. Review
  5. Ferroptosis in heart failure.Journal of molecular and cellular cardiology · 2022
    Review
  6. Review
  7. Article
  8. Perspectives on current models of Friedreich's ataxia.Frontiers in cell and developmental biology · 2022
    Article
  9. Article
  10. Article
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 1 country.

Alessandra BolottaDepartment of Experimental, Diagnostic and Specialty Medicine, Bologna University, 40126 Bologna, Italy.ORCID 0000-0002-7484-3452
Provvidenza Maria AbruzzoDepartment of Experimental, Diagnostic and Specialty Medicine, Bologna University, 40126 Bologna, Italy.ORCID 0000-0001-5242-9448
Vito Antonio BaldassarroInterdepartmental Centre for Industrial Research in Health Sciences and Technologies (ICIR-HST), University of Bologna, 40064 Ozzano, Bologna, Italy.ORCID 0000-0003-1020-4261
Alessandro GhezzoDepartment of Experimental, Diagnostic and Specialty Medicine, Bologna University, 40126 Bologna, Italy.ORCID 0000-0002-7928-1882
Katia ScotlandiCRS Development of Biomolecular Therapies, Experimental Oncology Laboratory, Orthopedic Rizzoli Institute, 40136 Bologna, Italy.
Marina MariniDepartment of Experimental, Diagnostic and Specialty Medicine, Bologna University, 40126 Bologna, Italy.ORCID 0000-0003-1932-7380
Cinzia ZucchiniDepartment of Experimental, Diagnostic and Specialty Medicine, Bologna University, 40126 Bologna, Italy.ORCID 0000-0001-7756-3838
Don Carlo Gnocchi Foundation · ITUniversity of Bologna · ITIstituto Ortopedico Rizzoli · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron homeostasis in the cardiac tissue as well as the involvement of the hepcidin-ferroportin (HAMP-FPN) axis in this process and in cardiac functionality are not fully understood. Imbalance of iron homeostasis occurs in several cardiac diseases, including iron-overload cardiomyopathies such as Friedreich's ataxia (FRDA, OMIM no. 229300), a hereditary neurodegenerative disorder. Exploiting the induced pluripotent stem cells (iPSCs) technology and the iPSC capacity to differentiate into specific cell types, we derived cardiomyocytes of a FRDA patient and of a healthy control subject in order to study the cardiac iron homeostasis and the HAMP-FPN axis. Both CTR and FRDA iPSCs-derived cardiomyocytes express cardiac differentiation markers; in addition, FRDA cardiomyocytes maintain the FRDA-like phenotype. We found that FRDA cardiomyocytes show an increase in the protein expression of HAMP and FPN. Moreover, immunofluorescence analysis revealed for the first time an unexpected nuclear localization of FPN in both CTR and FRDA cardiomyocytes. However, the amount of the nuclear FPN was less in FRDA cardiomyocytes than in controls. These and other data suggest that iron handling and the HAMP-FPN axis regulation in FRDA cardiac cells are hampered and that FPN may have new, still not fully understood, functions. These findings underline the complexity of the cardiac iron homeostasis.

Indexed as

CardiomyopathiesCation Transport ProteinsFerroportinFriedreich AtaxiaHepcidinsHumansInduced Pluripotent Stem CellsIronMyocytes, CardiacCation Transport ProteinsFerroportinHAMP protein, humanHepcidinsIron

Identifiers

PMID31049138
PMCPMC6458886
OpenAlexW2923093163

What OpenQuestion holds

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LicenceCC BY
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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.