ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Mitochondrial Transplantation Augments the Reparative Capacity of Macrophages Following Myocardial Injury.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- SIRT3 in post-myocardial infarction macrophage reprogramming: linking mitochondrial fitness to inflammation resolution and repair.Frontiers in immunology · 2026Pooled it
- Mitochondria-derived peptide hydrogel augments mitochondrial transplantation for promoting cardiac repair via macrophage metabolic reprogramming.Bioactive materials · 2027Article
- Injectable microsphere-based delivery strategies for stem cells and their derivatives in tissue regeneration.Bioactive materials · 2026Review
- Mitochondria-Targeted Nanotherapeutics: A Promising Strategy in Modulating Mitochondrial Function, Transfer, and Transplantation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Mitochondria-transplanted macrophages: a novel strategy targeting mitochondrial dysfunction to enhance myocardial repair after myocardial infarction.MedScience · 2026Article
- Polysaccharide-engineered mitochondria reprogram macrophages to resolve diabetic wound inflammation and promote repair.Bioactive materials · 2026Article
- Mitochondria as the Hub of Apoptosis: A Comprehensive Insight From Mitochondria to Interactions With Other Organelles.MedComm · 2026Review
- Eradication of MRSA biofilm-associated implant infections by low-immunogenic sustained-release lysostaphin fused to thermosensitive polypeptides.Nature communications · 2026Article
- Bioinspired Artificial Bioenergetic Organelles: Design Principles, Nanofabrication and Therapeutic Translation.Advanced materials (Deerfield Beach, Fla.) · 2026Review
- Microglial Mitochondrial Dysfunction: The Storm Center of Post-Stroke Neuroinflammation.CNS neuroscience & therapeutics · 2026Review
- Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats.Journal of orthopaedic translation · 2026Article
- From targeted delivery to inflammation suppression: engineering plant exosomes for heart failure therapy post-infarction.Materials today. Bio · 2026Article
- Preliminary exploration of the role of CD8Biomedical reports · 2026Article
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
- Research progress on the effects of M1/M2 macrophages on the differentiation and maturation of stem cell-derived cardiomyocytes: a review.Stem cell research & therapy · 2026Review
- Mitochondrial transfer as a driver of immune microenvironment remodeling.Frontiers in immunology · 2026Review
- Mitochondria transplantation mitigates attenuation of muscle fiber regeneration by evoked contractions.American journal of physiology. Cell physiology · 2026Article
- Mitochondrial Permeability Transition Pore: The Cardiovascular Disease's Molecular Achilles Heel.Biomedicines · 2025Review
- Mitochondrial Transplantation Augments the Reparative Capacity of Macrophages Following Myocardial Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiac Development, Cellular Composition and Function: From Regulatory Mechanisms to Applications.Cells · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The pathologically remodeled myocardial ischemic microenvironment, characterized by sustained hypoxia, metabolic insufficiency, and accumulation of inflammatory mediators, severely disrupts mitochondrial homeostasis. This dysfunction establishes a self-perpetuating cycle that impairs the coordinated healing cascade and compromises cardiac tissue repair following myocardial infarction (MI). To counteract these effects, a novel strategy of mitochondrial augmentation is proposed, whereby healthy exogenous mitochondria are introduced into macrophages to generate mitochondria-transplanted macrophages (Mito-T-Macros or MTMs), which can resist post-MI stress. Mitochondrial transplantation (MT) effectively induces macrophage polarization toward a reparative M2-like phenotype, thereby enhancing pro-healing functions, including migration, invasion, and phagocytosis. In vivo, MTM therapy enhances cardiac function after MI and attenuates left ventricular remodeling by reducing fibrosis, limiting apoptosis, and promoting angiogenesis. Mechanistically, MT accelerates the phenotypic transition of macrophages to a reparative state and prolongs their activity during the healing phase. Notably, a portion of the transplanted mitochondria are released from MTMs and subsequently internalized by cardiomyocytes, suggesting an additional mechanism of myocardial support. Overall, MT enhances the reparative capabilities of macrophages and contributes to the therapeutic efficacy of MTMs in ameliorating post-MI cardiac remodeling. These findings support MTM therapy as a promising and innovative approach for repairing myocardial injury following MI.
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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.