Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing 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.
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
30 authors.
Tasneem QaqorhDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-3506-5870
Yusuke TakahashiDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Kohei SameshimaDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0009-0006-4620-5214
Kentaro OtaniDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0001-7607-8056
Issei YazawaDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.
Yuya NishidaDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-1994-0807
Kohei TonaiDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0003-3410-859X
Yoshitaka FujiharaDepartment of Advanced Medical Technologies, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0001-8332-3507
Mizuki HondaDepartment of Drug Discovery Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID 0000-0003-3988-0802
Shinya OkiDepartment of Drug Discovery Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID 0000-0002-4767-3259
Yasuyuki OhkawaDivision of Transcriptomics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.ORCID 0000-0001-6440-9954
David R ThorburnMurdoch Children's Research Institute, Royal Children's Hospital, and University of Melbourne, Department of Paediatrics, Parkville, Victoria, Australia.ORCID 0000-0002-7725-9470
Ann E FrazierMurdoch Children's Research Institute, Royal Children's Hospital, and University of Melbourne, Department of Paediatrics, Parkville, Victoria, Australia.ORCID 0000-0002-6491-3437
Atsuhito TakedaDepartment of Pediatrics, Faculty of Medicine, Hokkaido University, Sapporo, Japan.
Yoshihiko IkedaDepartment of Pathology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0001-6395-5072
Heima SakaguchiDepartment of Pediatric Cardiology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-7758-840X
Takuya WatanabeDepartment of Transplant Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-9166-1749
Norihide FukushimaDepartment of Transplant Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0003-1367-4066
Yasumasa TsukamotoDepartment of Transplant Medicine, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-0963-6940
Naomasa MakitaOmics Research Center, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-1807-672X
Osamu YamaguchiOmics Research Center, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0002-7461-369X
Kei MurayamaDepartment of Metabolism, Chiba Children's Hospital, Chiba, Japan.ORCID 0000-0002-3923-8636
Akira OhtakeDepartment of Pediatrics and Clinical Genomics, Saitama Medical University, Moroyama, Saitama, Japan.ORCID 0000-0003-1147-3113
Yasushi OkazakiDiagnostics and Therapeutic of Intractable Diseases, Intractable Disease Research Center, Graduate School of Medicine, Juntendo University, Tokyo, Japan.ORCID 0000-0003-3241-5502
Takanari KimuraDepartment of Medical Biochemistry, Osaka University Graduate School of Frontier Biosciences, Suita, Osaka, Japan.
Hisakazu KatoDepartment of Medical Biochemistry, Osaka University Graduate School of Frontier Biosciences, Suita, Osaka, Japan.ORCID 0000-0003-4619-3680
Hijiri InoueDepartment of Medical Biochemistry, Osaka University Graduate School of Frontier Biosciences, Suita, Osaka, Japan.
Ken MatsuokaDepartment of Medical Biochemistry, Osaka University Graduate School of Frontier Biosciences, Suita, Osaka, Japan.
Seiji TakashimaDepartment of Medical Biochemistry, Osaka University Graduate School of Frontier Biosciences, Suita, Osaka, Japan.
Yasunori ShintaniDepartment of Molecular Pharmacology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan.ORCID 0000-0001-9579-0727
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
Oxidative phosphorylation defects result in now intractable mitochondrial diseases (MD) with cardiac involvement markedly affecting prognosis. The mechanisms underlying the transition from compensation to dysfunction in response to metabolic deficiency remain unclear. Here, we used spatially resolved transcriptomics and single-nucleus RNA sequencing (snRNA-seq) on the heart of a patient with mitochondrial cardiomyopathy (MCM), combined with an MCM mouse model with cardiac-specific Ndufs6 knockdown (FS6KD). Cardiomyocytes demonstrated the most heterogeneous expression landscape among cell types caused by metabolic perturbation, and pseudotime trajectory analysis revealed dynamic cellular states transitioning from compensation to severe compromise. This progression coincided with the transient up-regulation of a transcription factor,
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.
Atf3 controls transitioning in female mitochondrial cardiomyopathy as identified by spatial and single-cell transcriptomics. · full record | OpenQuestion