ArticleInternational journal of molecular sciences2021
Mitochondrial Transfer Improves Cardiomyocyte Bioenergetics and Viability in Male Rats Exposed to Pregestational Diabetes.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Mitochondria transfer research from cellular mechanisms to immune-inflammatory and translational frontiers: a bibliometric analysis from 2006 to 2026.Frontiers in immunology · 2026Pooled it
- RNA-Based Therapies for Treating Monogenic Cardiomyopathies.The Canadian journal of cardiology · 2026Review
- Intercellular Mitochondrial Transfer: Implications in Cardiovascular Health.Circulation research · 2026Review
- Mitochondrial Transfer: From Bench to Bedside.Circulation research · 2026Review
- From the energy factory to the intercellular communication medium: the emerging role of intercellular mitochondrial transfer and mitochondrial transplantation therapy in diabetes and diabetic complications.Journal of translational medicine · 2026Review
- Article
- The Transgenerational Impact of High-Fat Diet and Diabetic Pregnancy on Embryonic Transcriptomics and Mitochondrial Health.Biomedicines · 2025Article
- The mechanism of maternal inheritance of glycolipid metabolism disorder in a zebrafish model of type 2 diabetes.Scientific reports · 2025Article
- Targeting mitochondrial transfer: a new horizon in cardiovascular disease treatment.Journal of translational medicine · 2024Review
- Gestational Diabetes-like Fuels Impair Mitochondrial Function and Long-Chain Fatty Acid Uptake in Human Trophoblasts.International journal of molecular sciences · 2024Article
- Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update.Molecular neurobiology · 2024Review
- Polymer-Functionalized Mitochondrial Transplantation to Fibroblasts Counteracts a Pro-Fibrotic Phenotype.International journal of molecular sciences · 2023Article
- Mitochondrial Transfer as a Novel Therapeutic Approach in Disease Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- The Mighty NUMT: Mitochondrial DNA Flexing Its Code in the Nuclear Genome.Biomolecules · 2023Review
- Remodeling of Mitochondria in Cancer and Other Diseases.International journal of molecular sciences · 2023Article
- Mitochondria on the move: Horizontal mitochondrial transfer in disease and health.The Journal of cell biology · 2023Article
- Impact of Prenatal Exposure to Maternal Diabetes and High-Fat Diet on Postnatal Myocardial Ketone Body Metabolism in Rats.International journal of molecular sciences · 2023Article
- Mitochondrial transfer - a novel promising approach for the treatment of metabolic diseases.Frontiers in endocrinology · 2023Review
- Long-term outcomes and potential mechanisms of offspring exposed to intrauterine hyperglycemia.Frontiers in nutrition · 2023Review
- Transcriptomic and proteomic pathways of diabetic and non-diabetic mitochondrial transplantation.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Offspring born to diabetic or obese mothers have a higher lifetime risk of heart disease. Previously, we found that rat offspring exposed to late-gestational diabetes mellitus (LGDM) and maternal high-fat (HF) diet develop mitochondrial dysfunction, impaired cardiomyocyte bioenergetics, and cardiac dysfunction at birth and again during aging. Here, we compared echocardiography, cardiomyocyte bioenergetics, oxidative damage, and mitochondria-mediated cell death among control, pregestational diabetes mellitus (PGDM)-exposed, HF-diet-exposed, and combination-exposed newborn offspring. We hypothesized that PGDM exposure, similar to LGDM, causes mitochondrial dysfunction to play a central, pathogenic role in neonatal cardiomyopathy. We found that PGDM-exposed offspring, similar to LGDM-exposed offspring, have cardiac dysfunction at birth, but their isolated cardiomyocytes have seemingly less bioenergetics impairment. This finding was due to confounding by impaired viability related to poorer ATP generation, more lipid peroxidation, and faster apoptosis under metabolic stress. To mechanistically isolate and test the role of mitochondria, we transferred mitochondria from normal rat myocardium to control and exposed neonatal rat cardiomyocytes. As expected, transfer provides a respiratory boost to cardiomyocytes from all groups. They also reduce apoptosis in PGDM-exposed males, but not in females. Findings highlight sex-specific differences in mitochondria-mediated mechanisms of developmentally programmed heart disease and underscore potential caveats of therapeutic mitochondrial transfer.
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Registered trials
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.