Mitochondrial dynamics and transfer in mesenchymal stromal cells: Redox regulation, therapeutic mechanisms, and engineering strategies.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing preclinical mechanisms and engineering strategies without new human clinical data.
PubMed 42167417 · doi:10.1016/j.freeradbiomed.2026.05.291
What was done
This narrative review synthesized preclinical literature on mesenchymal stromal cell (MSC) mitochondrial biology and intercellular mitochondrial transfer. It examined cellular mechanisms including metabolic reprogramming, fusion-fission dynamics, mitophagy, redox signaling pathways (such as ROS production and Nrf2/Keap1 signaling), post-translational modifications of transfer machinery (including connexin 43 and Miro1), and transfer routes across various disease models.
What was found
The abstract reports no quantitative data or numerical outcomes. It describes qualitatively that MSCs transfer functional mitochondria to damaged cells via tunneling nanotubes, connexin 43 communication, and extracellular vesicles, which preserves ATP production, reduces oxidative injury, and remodels immunometabolic phenotypes across preclinical models of pulmonary, cardiovascular, neurological, renal, hepatic, and immune-mediated conditions.
Why it matters
This review integrates redox regulation with intercellular mitochondrial transfer biology to outline potential targets and bioengineering approaches for MSC-based regenerative therapies.
Limits
The conclusions are derived from narrative synthesis of preclinical in vitro and animal models with no new human clinical trial data. No search syntax, study selection criteria, or risk-of-bias evaluations are provided. Significant translational challenges including cell heterogeneity, dosing, in vivo tracking, and long-term biosafety remain uncharacterized in humans.
Cited by
- supports Stem cells are capable of replacing damaged organelles, such as mitochondria, in other cells.