ArticleJournal of cellular and molecular medicine2020
TAT-dextran-mediated mitochondrial transfer enhances recovery from models of reperfusion injury in cultured cardiomyocytes.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 65 citations in OpenAlex.
- Novel Allogeneic Mitochondria and Associated Organelle Complex Treatment Prevents Myocardial Ischemia-Reperfusion Injury Through Anti-Apoptotic Effects.JACC. Asia · 2026Article
- Mitochondrial Transplantation Therapy for Ischemic Stroke: Progress and Challenges.Cellular and molecular neurobiology · 2026Review
- Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Biotechnological approaches and therapeutic potential of mitochondria transfer and transplantation.Nature communications · 2025Review
- Therapeutic implications of mitochondrial transfer on stem cell fate in regenerative medicine.Journal of translational medicine · 2025Review
- Engineered mitochondria in diseases: mechanisms, strategies, and applications.Signal transduction and targeted therapy · 2025Review
- Autologous mitochondrial transplantation enhances the bioenergetics of auditory cells and mitigates cell loss induced by HMitochondrion · 2025Article
- Nanoengineered mitochondria enable ocular mitochondrial disease therapyActa pharmaceutica Sinica. B · 2024Article
- Unveiling the power of mitochondrial transfer in cancer progression: a perspective in ovarian cancer.Journal of ovarian research · 2024Review
- Mitochondrial transplantation: a promising strategy for treating degenerative joint diseases.Journal of translational medicine · 2024Review
- Mitochondrial Transportation, Transplantation, and Subsequent Immune Response in Alzheimer's Disease: An Update.Molecular neurobiology · 2024Review
- The relationship between cardiac oxidative stress, inflammatory cytokine response, cardiac pump function, and prognosis post-myocardial infarction.Scientific reports · 2024Article
- Association with cationized gelatin nanospheres enhances cell internalization of mitochondria efficiency.Regenerative therapy · 2023Article
- Highly Specialized Mechanisms for Mitochondrial Transport in Neurons: From Intracellular Mobility to Intercellular Transfer of Mitochondria.Biomolecules · 2023Review
- Mitochondrial transplantation as a novel therapeutic strategy for cardiovascular diseases.Journal of translational medicine · 2023Review
- Mitochondrial Transfer as a Novel Therapeutic Approach in Disease Diagnosis and Treatment.International journal of molecular sciences · 2023Review
- Emerging Landscape of Cell-Penetrating Peptide-Mediated Organelle Restoration and Replacement.ACS pharmacology & translational science · 2023Review
- Mitochondrial Transplantation in Mitochondrial Medicine: Current Challenges and Future Perspectives.International journal of molecular sciences · 2023Review
- Preferred Migration of Mitochondria toward Cells and Tissues with Mitochondrial Damage.International journal of molecular sciences · 2022Article
- The Therapeutic Strategies Targeting Mitochondrial Metabolism in Cardiovascular Disease.Pharmaceutics · 2022Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myocardial infarction is a leading cause of death among single organ diseases. Despite successful reperfusion therapy, ischaemia reperfusion injury (IRI) can induce oxidative stress (OS), cardiomyocyte apoptosis, autophagy and release of inflammatory cytokines, resulting in increased infarct size. In IRI, mitochondrial dysfunction is a key factor, which involves the production of reactive oxygen species, activation of inflammatory signalling cascades or innate immune responses, and apoptosis. Therefore, intercellular mitochondrial transfer could be considered as a promising treatment strategy for ischaemic heart disease. However, low transfer efficiency is a challenge in clinical settings. We previously reported uptake of isolated exogenous mitochondria into cultured cells through co-incubation, mediated by macropinocytosis. Here, we report the use of transactivator of transcription dextran complexes (TAT-dextran) to enhance cellular uptake of exogenous mitochondria and improve the protective effect of mitochondrial replenishment in neonatal rat cardiomyocytes (NRCMs) against OS. TAT-dextran-modified mitochondria (TAT-Mito) showed a significantly higher level of cellular uptake. Mitochondrial transfer into NRCMs resulted in anti-apoptotic capability and prevented the suppression of oxidative phosphorylation in mitochondria after OS. Furthermore, TAT-Mito significantly reduced the apoptotic rates of cardiomyocytes after OS, compared to simple mitochondrial transfer. These results indicate the potential of mitochondrial replenishment therapy in OS-induced myocardial IRI.
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