ArticleInternational journal of molecular sciences2023
Polymer-Functionalized Mitochondrial Transplantation to Fibroblasts Counteracts a Pro-Fibrotic Phenotype.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Nanomedicine beyond carriers - devices, cells & living therapeutics.Biomedical microdevices · 2026Review
- Mitochondrial transfer: a novel paradigm for wound healing.Burns & trauma · 2026Review
- Mitochondrial transplantation for osteoarthritis: from molecular mechanisms to clinical translation.Frontiers in immunology · 2026Review
- Plasma-derived mitochondria as a minimal manipulation alternative for attenuating inflammatory immune responses.Regenerative biomaterials · 2026Article
- The regulation of placental pericyte function through transforming growth factor β-1 signalling.Scientific reports · 2025Article
- Biotechnological approaches and therapeutic potential of mitochondria transfer and transplantation.Nature communications · 2025Review
- Nuclear respiratory factor-1 (NRF1) induction as a powerful strategy to deter mitochondrial dysfunction and senescence in mesenchymal stem cells.Aging cell · 2025Article
- Citrus pectin-coated inhalable PLGA nanoparticles for treatment of pulmonary fibrosis.Journal of materials chemistry. B · 2025Article
- Engineered mitochondria in diseases: mechanisms, strategies, and applications.Signal transduction and targeted therapy · 2025Review
- Nuclear respiratory factor-1 (NRF1) induction drives mitochondrial biogenesis and attenuates amyloid beta-induced mitochondrial dysfunction and neurotoxicity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Identification of glycolysis-related gene signatures for prognosis and therapeutic targeting in idiopathic pulmonary fibrosis.Frontiers in pharmacology · 2025Article
- Recent advances in mitochondrial transplantation to treat disease.Biomaterials translational · 2025Review
- Identification of glycolysis-related clusters and immune cell infiltration in hepatic fibrosis progression using machine learning models and experimental validation.Frontiers in immunology · 2025Article
- Mitochondrial transplantation: a promising strategy for treating degenerative joint diseases.Journal of translational medicine · 2024Review
- The diagnostic value and associated molecular mechanism study for fibroblast-related mitochondrial genes on keloid.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Bicyclol attenuates pulmonary fibrosis with silicosis via both canonical and non-canonical TGF-β1 signaling pathways.Journal of translational medicine · 2024Article
- Mitochondria as a therapeutic: a potential new frontier in driving the shift from tissue repair to regeneration.Regenerative biomaterials · 2023Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
Fibroblast-to-myofibroblast transition (FMT) leads to excessive extracellular matrix (ECM) deposition-a well-known hallmark of fibrotic disease. Transforming growth factor-β (TGF-β) is the primary cytokine driving FMT, and this phenotypic conversion is associated with mitochondrial dysfunction, notably a metabolic reprogramming towards enhanced glycolysis. The objective of this study was to examine whether the establishment of favorable metabolic phenotypes in TGF-β-stimulated fibroblasts could attenuate FMT. The hypothesis was that mitochondrial replenishment of TGF-β-stimulated fibroblasts would counteract a shift towards glycolytic metabolism, consequently offsetting pro-fibrotic processes. Isolated mitochondria, functionalized with a dextran and triphenylphosphonium (TPP) (Dex-TPP) polymer conjugate, were administered to fibroblasts (MRC-5 cells) stimulated with TGF-β, and effects on bioenergetics and fibrotic programming were subsequently examined. Results demonstrate that TGF-β stimulation of fibroblasts led to FMT, which was associated with enhanced glycolysis. Dex-TPP-coated mitochondria (Dex-TPP/Mt) delivery to TGF-β-stimulated fibroblasts abrogated a metabolic shift towards glycolysis and led to a reduction in reactive oxygen species (ROS) generation. Importantly, TGF-β-stimulated fibroblasts treated with Dex-TPP/Mt had lessened expression of FMT markers and ECM proteins, as well as reduced migration and proliferation. Findings highlight the potential of mitochondrial transfer, as well as other strategies involving functional reinforcement of mitochondria, as viable therapeutic modalities in fibrosis.
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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.