Article in Circulation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing 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
9 authors.
Yoshinobu NakayamaDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, City College of New York, New York, NY (Y.N., A.M., S.A.A.,A.M.P.B.S., J.Y.).ORCID 0000-0002-0818-4145
Satoru KobayashiDepartment of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY (S.K., Q.L.).ORCID 0000-0003-4390-5726
Aliya MasihuddinDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, City College of New York, New York, NY (Y.N., A.M., S.A.A.,A.M.P.B.S., J.Y.).
Syed Amir AbdaliDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, City College of New York, New York, NY (Y.N., A.M., S.A.A.,A.M.P.B.S., J.Y.).
A M Pramodh Bandara SeneviratneDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, City College of New York, New York, NY (Y.N., A.M., S.A.A.,A.M.P.B.S., J.Y.).ORCID 0000-0002-1250-5861
Sachiyo IshiiDepartment of Anesthesiology and Critical Care, Kyoto Prefectural University of Medicine, Kyoto, Japan (S.I., J.I.).
Jun IidaDepartment of Anesthesiology and Critical Care, Kyoto Prefectural University of Medicine, Kyoto, Japan (S.I., J.I.).
Qiangrong LiangDepartment of Biomedical Sciences, New York Institute of Technology College of Osteopathic Medicine, Old Westbury, NY (S.K., Q.L.).ORCID 0000-0002-6123-5685
Jun YoshiokaDepartment of Molecular, Cellular and Biomedical Sciences, City University of New York School of Medicine, City College of New York, New York, NY (Y.N., A.M., S.A.A.,A.M.P.B.S., J.Y.).ORCID 0000-0002-7176-3414
Funding
Research Center in Minority Institutions (RCMI) at City CollegeU54MD017979 · NIMHD · CITY COLLEGE OF NEW YORK · PI M. Felice Marina GHILARDI · 2024 to 2026
$15.9M
Arrestin domain-containing protein 4 as a novel regulator of glucose metabolism in the ischemic heartR01HL166620 · NHLBI · CITY COLLEGE OF NEW YORK · PI Jun Yoshioka · 2023 to 2026
$1.6M
Hyperglycemia-induced regulatory mechanism of ER stress by arresting domain-containing protein 4 in diabetic cardiomyopathyR01HL168191 · NHLBI · CITY COLLEGE OF NEW YORK · PI Jun Yoshioka · 2024 to 2026
$1.2M
Deciphering the role of lysosomal membrane permeabilization in Diabetic Cardiac InjuryR15HL161737 · NHLBI · NEW YORK INST OF TECHNOLOGY · PI KOBAYASHI, SATORU · 2022 to 2022
$428k
Deciphering the Role of AMPK in Doxorubicin CardiotoxicityR15HL163707 · NHLBI · NEW YORK INST OF TECHNOLOGY · PI LIANG, QIANGRONG · 2023 to 2023
backgroundExercise intolerance is an independent predictor of poor prognosis in diabetes. The underlying mechanism of the association between hyperglycemia and exercise intolerance remains undefined. We recently demonstrated that the interaction between ARRDC4 (arrestin domain-containing protein 4) and GLUT1 (glucose transporter 1) regulates cardiac metabolism.
methodsTo determine whether this mechanism broadly impacts diabetic complications, we investigated the role of ARRDC4 in the pathogenesis of diabetic cardiac/skeletal myopathy using cellular and animal models.
resultsHigh glucose promoted translocation of MondoA into the nucleus, which upregulated
conclusionsARRDC4 regulates hyperglycemia-induced toxicities toward cardiac and skeletal muscle, revealing a new molecular framework that connects hyperglycemia to cardiac/skeletal myopathy to exercise intolerance.
Indexed as
Exercise ToleranceGlucose Transporter Type 1Mice, KnockoutAnimalsCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic CardiomyopathiesHumansHyperglycemiaIntracellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMuscle, SkeletalMyocytes, CardiacArrdc4 protein, mouseGlucose Transporter Type 1Intracellular Signaling Peptides and ProteinsSlc2a1 protein, mouseadaptor proteindiabetic cardiomyopathyenergy metabolismexercise endurancehealth
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.
Systemic Deletion of ARRDC4 Improves Cardiac Reserve and Exercise Capacity in Diabetes. · full record | OpenQuestion