ArticleCirculation research2018
Transplanted Mesenchymal Stem Cells Reduce Autophagic Flux in Infarcted Hearts via the Exosomal Transfer of miR-125b.
Article in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 169 papers, 5 of them syntheses that pooled it.
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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
169 citing papers in PubMed, 5 syntheses or guidelines pooled it, 306 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- A systematic review on the role of MSC-derived exosomal miRNAs in the treatment of heart failure.Molecular biology reports · 2022Pooled it
- Stem cell-derived exosomes in the treatment of acute myocardial infarction in preclinical animal models: a meta-analysis of randomized controlled trials.Stem cell research & therapy · 2022Pooled it
- Mesenchymal Stem Cell Exosomes in the Treatment of Myocardial Infarction: a Systematic Review of Preclinical In Vivo Studies.Journal of cardiovascular translational research · 2022Pooled it
- Extracellular Vesicles as a Cell-free Therapy for Cardiac Repair: a Systematic Review and Meta-analysis of Randomized Controlled Preclinical Trials in Animal Myocardial Infarction Models.Stem cell reviews and reports · 2022Pooled it
- Exosomes derived from AHR-overexpressing human umbilical cord mesenchymal stem cells attenuate H/R injury via AHR/NLRP3 pathway.Cell cycle (Georgetown, Tex.) · 2026Article
- Empagliflozin-pretreated mesenchymal stem cell-derived extracellular vesicles facilitate cardiac repair via AGGF1.Journal of nanobiotechnology · 2026Article
- Mesenchymal stem cell exosomes alleviate ischemic myocardial injury by miR-125b-5p/BTG2 pathway.Molecular and cellular biochemistry · 2026Article
- MSC-Derived Exosomes in Preserving Autophagy through Key Signaling Pathways: A Preventive Strategy against Cardiovascular Aging.Cell biochemistry and biophysics · 2026Review
- Small vesicles, big potential: A review of innovative exosome delivery and molecular mechanisms in preclinical myocardial infarction models.Animal models and experimental medicine · 2026Review
- ERVWE1 Impairs Mitochondrial Homeostasis and Promotes Neuronal Apoptosis via the miR-27b-3p/BNIP3 Axis in Schizophrenia.Viruses · 2026Article
- Mesenchymal Stem Cell-Derived Exosomes: A Tool for Heart Failure Repair - From Molecular Mechanisms to Clinical Potential.Journal of inflammation research · 2026Review
- Mesenchymal stem cell-derived exosomes in myocardial infarction repair: therapeutic potential and scaffold-based delivery strategies.Frontiers in pharmacology · 2026Review
- miRNAs from mesenchymal-stem-cell-derived extracellular vesicles: Emerging players in regenerative medicine and disease therapy.Molecular therapy. Nucleic acids · 2025Review
- The Impact of Opioids on Epigenetic Modulation in Myocardial Ischemia and Reperfusion Injury: Focus on Non-coding RNAs.Journal of cardiovascular translational research · 2025Review
- TNF-α-preconditioning enhances analgesic efficacy of mesenchymal stem cell-derived extracellular vesicle in neuropathic painBioactive materials · 2025Article
- Empagliflozin-pretreated BMSC exosomes attenuate myocardial ischemia-reperfusion injury by enhancing atad3a/pink1-dependent mitophagy.Stem cell research & therapy · 2025Article
- miR-125b-5p and miR-145a-5p modulation drives functional enhancement of Wharton's Jelly-MSCs derived small extracellular vesicles in response to hypoxia preconditioning.Cell communication and signaling : CCS · 2025Article
- METTL3-dependent mAutophagy · 2025Article
- Cardiac repair and regeneration: cell therapy, in vivo reprogramming, and the promise of extracellular vesicles.Experimental & molecular medicine · 2025Review
109 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleAutophagy can preserve cell viability under conditions of mild ischemic stress by degrading damaged organelles for ATP production, but under conditions of severe ischemia, it can promote cell death and worsen cardiac performance. Mesenchymal stem cells (MSCs) are cardioprotective when tested in animal models of myocardial infarction, but whether these benefits occur through the regulation of autophagy is unknown.
objectiveTo determine whether transplanted MSCs reduce the rate of autophagic degradation (autophagic flux) in infarcted hearts and if so, to characterize the mechanisms involved. METHODS AND
resultsTreatment with transplanted MSCs improved cardiac function and infarct size while reducing apoptosis and measures of autophagic flux (bafilomycin A1-induced LC3-II [microtubule-associated protein 1 light chain 3] accumulation and autophagosome/autolysosome prevalence) in infarcted mouse hearts. In hypoxia and serum deprivation-cultured neonatal mouse cardiomyocytes, autophagic flux and cell death, as well as p53-Bnip3 (B-cell lymphoma 2-interacting protein 3) signaling, declined when the cells were cultured with MSCs or MSC-secreted exosomes (MSC-exo), but the changes associated with MSC-exo were largely abolished by pretreatment with the exosomal inhibitor GW4869. Furthermore, a mimic of the exosomal oligonucleotide miR-125b reduced, whereas an anti-miR-125b oligonucleotide increased, autophagic flux and cell death, via modulating p53-Bnip3 signaling in hypoxia and serum deprivation-cultured neonatal mouse cardiomyocytes. In the in vivo mouse myocardial infarction model, MSC-exo, but not the exosomes obtained from MSCs pretreated with the anti-miR-125b oligonucleotide (MSC-exo
conclusionsThe beneficial effects offered by MSC transplantation after myocardial infarction are at least partially because of improved autophagic flux through excreted exosome containing mainly miR-125b-5p.
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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.