ArticleThe Journal of clinical investigation2023
1-Deoxynojirimycin promotes cardiac function and rescues mitochondrial cristae in mitochondrial hypertrophic cardiomyopathy.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Activity-based proteomics analysis revealed that DNJ directly targeted ATP5F1 to alleviate high glucose induced cardiomyocyte injury.Cell communication and signaling : CCS · 2026Article
- Cellular and Molecular Mechanisms of Heart Failure and Sudden Cardiac Death in Hypertrophic Cardiomyopathy and Methods Used for Their Pathogenetic Correction.Biomedicines · 2025Review
- Mitochondrial Quality Control and Cell Death.International journal of molecular sciences · 2025Review
- AI662270/GRP94 axis couples the unfolded protein response to mitochondrial dynamics during acute myocardial infarction.JCI insight · 2025Article
- Precision Medicine: Therapeutically Targeting Mitochondrial Alterations in Heart Failure.JACC. Basic to translational science · 2025Review
- Insights into the Activities and Usefulness of Deoxynojirimycin andMolecules (Basel, Switzerland) · 2025Review
- The silkworm: A promising invertebrate diabetes model for natural drug discovery.Global health & medicine · 2025Review
- Effect of 1-DNJ on Oxidative Stress-Induced Apoptosis in Porcine Ovarian GCs Through Modulation of the PERK-ATF4/MFN2 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Hypertrophic Cardiomyopathy Through the Lens of Mitochondria.Biomedicines · 2025Review
- Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis.Current issues in molecular biology · 2025Article
- Astragalus polyphenols attenuates doxorubicin-induced cardiotoxicity by activating the PI3K/AKT/NRF2 pathway.PloS one · 2025Article
- Transcriptomic analysis and machine learning modeling identifies novel biomarkers and genetic characteristics of hypertrophic cardiomyopathy.Frontiers in genetics · 2025Article
- Social survey on knowledge, attitude and practice of hypertrophic cardiomyopathy.Frontiers in cardiovascular medicine · 2025Article
- Effects of 1-Deoxynojirimycin Extracts of Mulberry Leaves on Oxidative Stress and the Function of the Intestinal Tract in Broilers Induced by HAnimals : an open access journal from MDPI · 2024Article
- Clinical trials in-a-dish for cardiovascular medicine.European heart journal · 2024Review
- Genetic Mutations and Mitochondrial Redox Signaling as Modulating Factors in Hypertrophic Cardiomyopathy: A Scoping Review.International journal of molecular sciences · 2024Article
- Sudden Cardiac Death in the Young: State-of-the-Art Review in Molecular Autopsy.Current issues in molecular biology · 2024Review
- Preserving mitochondria to treat hypertrophic cardiomyopathy: From rare mitochondrial DNA mutation to heart failure therapy?The Journal of clinical investigation · 2023Article
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Authors and funding
25 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is the most prominent cause of sudden cardiac death in young people. Due to heterogeneity in clinical manifestations, conventional HCM drugs have limitations for mitochondrial hypertrophic cardiomyopathy. Discovering more effective compounds would be of substantial benefit for further elucidating the pathogenic mechanisms of HCM and treating patients with this condition. We previously reported the MT-RNR2 variant associated with HCM that results in mitochondrial dysfunction. Here, we screened a mitochondria-associated compound library by quantifying the mitochondrial membrane potential of HCM cybrids and the survival rate of HCM-induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) in galactose media. 1-Deoxynojirimycin (DNJ) was identified to rescue mitochondrial function by targeting optic atrophy protein 1 (OPA1) to promote its oligomerization, leading to reconstruction of the mitochondrial cristae. DNJ treatment further recovered the physiological properties of HCM iPSC-CMs by improving Ca2+ homeostasis and electrophysiological properties. An angiotensin II-induced cardiac hypertrophy mouse model further verified the efficacy of DNJ in promoting cardiac mitochondrial function and alleviating cardiac hypertrophy in vivo. These results demonstrated that DNJ could be a potential mitochondrial rescue agent for mitochondrial hypertrophic cardiomyopathy. Our findings will help elucidate the mechanism of HCM and provide a potential therapeutic strategy.
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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.