ArticleApoptosis : an international journal on programmed cell death2023
TFAM-Mediated mitochondrial transfer of MSCs improved the permeability barrier in sepsis-associated acute lung injury.
Article in Apoptosis : an international journal on programmed cell death, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 26 citations in OpenAlex.
- RHOT1/2-driven mitochondrial membrane vesicles confer tumor-homing selectivity and enable in situ cancer vaccination.Nature communications · 2026Article
- Microglial tunneling nanotubes: an intercellular transfer facilitating mitochondrial dysfunction and neuroinflammation in experimental cerebral malaria.Apoptosis : an international journal on programmed cell death · 2026Article
- Mitochondrial transfer between tumor and immune cells: a nexus of metabolic adaptation and immune dysfunction.Biomarker research · 2026Review
- The macrophage DAG/PKCα/ROS axis exacerbates sepsis by inducing endothelial dysfunction through activation of the p38 MAPK pathway.Molecular biology reports · 2026Article
- Mitochondrial Transfer to Endothelial Cells: Mechanisms, Evidence, and Therapeutic Potential.Circulation research · 2026Review
- Cumambrin B Alleviates Sepsis-Associated Acute Lung Injury by Activating the Nrf2/HO-1 Pathway.Biomedicines · 2026Article
- Cytoskeletal remodeling promotes tunneling nanotube formation and drives cardiac resident cell mitochondrial transfer in sepsis.Science advances · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026Review
- Emerging Roles and Possible Therapeutic Applications of Arachidonic Acid Metabolites in Sepsis and Sepsis-Associated Organ Dysfunction.Drug design, development and therapy · 2026Review
- The role of mitochondrial transfer in lung disease.Respiratory research · 2025Review
- Mesenchymal stromal cell-mediated mitochondrial transfer unveils new frontiers in disease therapy.Stem cell research & therapy · 2025Review
- Mesenchymal stem cell therapies for ARDS: translational promise and challenges.Stem cell research & therapy · 2025Review
- Mitochondrial Quality Control: Insights into Intracerebral Hemorrhage.Cellular and molecular neurobiology · 2025Review
- Dynamic three-dimensional culture enhances tunneling nanotubes-mediated mitochondrial transfer in mesenchymal stromal cells to accelerate wound healing.Journal of nanobiotechnology · 2025Article
- Review
- Mitochondrial transfer in endothelial cells and vascular health.Trends in cell biology · 2025Review
- Mitochondria Transfer in Mesenchymal Stem Cells: Unraveling the Mechanism and Therapeutic Potential.Current stem cell research & therapy · 2025Review
- Mitochondrial transfer/transplantation in lung injury: mechanism, therapeutic potential, and clinical application.Frontiers in immunology · 2025Review
- Gut microbiota dysbiosis aggravates sepsis-induced lung injury by promoting neutrophil extracellular traps and suppressing host integrin defense.Frontiers in microbiology · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial cell barrier disruption is a hallmark of sepsis-induced acute lung injury (ALI). Mesenchymal stem cells (MSCs)-based therapy has been regarded as a promising treatment for repairing injured lungs, and mitochondrial transfer was shown to be important for the therapeutic effects of MSCs. Here we investigated the ability of MSCs to modulate endothelial barrier integrity through mitochondrial transfer in sepsis-induced ALI. We found that mitochondrial transfer from MSCs to LPS-induced PMVECs through forming tunneling nanotubes (TNTs). Due to the inhibition of TNTs (using LAT-A), MSCs-mediated reparation on PMVECs functions, including cell apoptosis, MMP, ATP generation, TEER level and monolayer permeability of FITC-dextran were greatly inhibited. In addition, silencing of mitochondrial transcription factor A (TFAM) in MSCs could also partly inhibit the TNTs formation and aggravate the LPS-induced mitochondrial dysfunction and permeability barrier in PMVECs. Furthermore, the LPS-induced pulmonary edema and higher pulmonary vascular permeability were alleviated by MSCs while that of lung tissue bounced back after MSCs were pre-incubated by LAT-A and or down-regulation of TFAM. Therefore, we firstly revealed that regulation of TFAM expression in MSCs played a critical role to improve the permeability barrier of PMVECs by TNTs mediating mitochondrial transfer in sepsis-associated ALI. This study provided a new therapeutic strategy for the treatment of sepsis-induced ALI.
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