Evidence map›Paper›PMID 42033870›Full record

ArticleJACC. Basic to translational science2026

Inhibition of Cyclophilin D Rescues Cardiac Function and Bioenergetic Defects Caused by Neonatal Hypoxia.

Jonathan R Burris, Gisela Beutner, Min Yee, Bartholomew V Simon, Michael F Swartz, Kathryn B Boudreau, Ethan D Cohen, Chaitanya A Kulkarni, Prottoy Hasan, Hongyue Wang and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Cyclophilin D at the Heart of Neonatal Hypoxia.JACC. Basic to translational science · 2026
    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

17 authors.

Jonathan R BurrisDivision of Cardiology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA; Division of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA.
Gisela BeutnerDivision of Cardiology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA.
Min YeeDivision of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA.
Bartholomew V SimonDepartment of Surgery, University of Rochester Medical Center, Rochester, New York, USA.
Michael F SwartzDepartment of Surgery, University of Rochester Medical Center, Rochester, New York, USA.
Kathryn B BoudreauAab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA; Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, USA.
Ethan D CohenDivision of Cardiology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA; Division of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA.
Chaitanya A KulkarniDepartment of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, New York, USA.
Prottoy HasanDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Hongyue WangDepartment of Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, New York, USA.
Karen L de Mesy BentleyDepartment of Pathology and Laboratory Medicine and the Electron Microscope Resource, University of Rochester Medical Center, Rochester, New York, USA.
György HajnóczkyDepartment of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
George M AlfierisDepartment of Surgery, University of Rochester Medical Center, Rochester, New York, USA.
Eric M SmallAab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA; Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, USA.
Paul S BrookesAab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA; Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, USA; Department of Anesthesiology and Perioperative Medicine, University of Rochester Medical Center, Rochester, New York, USA.
Michael A O'ReillyDivision of Neonatology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA.
George A PorterDivision of Cardiology, Department of Pediatrics, University of Rochester Medical Center, Rochester, New York, USA; Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester Medical Center, Rochester, New York, USA; Department of Pharmacology and Physiology, University of Rochester Medical Center, Rochester, New York, USA. Electronic address: george_porter@urmc.rochester.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased oxygen levels at birth regulate myocyte bioenergetic and structural maturation controlled by mitochondrial cyclophilin D (CypD). We evaluated mechanisms of neonatal hypoxic cardiac dysfunction by exposing neonatal mice to 12% oxygen and studied cardiac bioenergetics, myocyte maturation, and function. Hypoxia decreased the activity/assembly of electron transport chain complex I, uncoupled oxidative phosphorylation, increased proliferation, decreased differentiation, increased ventricular mass, and decreased cardiac function. CypD inhibition rescued most hypoxia-mediated effects and increased cardiac function. In conclusion, neonatal hypoxia alters cardiac bioenergetics, myocyte maturation, and cardiac function through CypD-dependent pathways, providing potential therapeutic targets for neonatal cardiac dysfunction.

Indexed as

cardiac developmentcardiomyocyte maturationcyclosporin AmitochondriaNIM811

Identifiers

PMID42033870
PMCPMC13127397

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.