ArticleJournal of nanobiotechnology2021
Hemin enhances the cardioprotective effects of mesenchymal stem cell-derived exosomes against infarction via amelioration of cardiomyocyte senescence.
Article in Journal of nanobiotechnology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled 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
- circKIAA1462 impaires autophagy and promotes pyroptosis in retinal pigment epithelium via the miR-183-5p/HMGB1 axis in diabetic retinopathy.Journal of translational medicine · 2026Article
- Exosomes Enhance Diagnosis and Therapy of Ischemic Heart Disease: Insights and Advances.Journal of cardiovascular translational research · 2026Review
- Mesenchymal Stem Cell Secretome for Cardiac Regeneration: Opportunity for Cell-Free Therapy.International journal of molecular sciences · 2025Review
- PBX1 promotes osteoporosis by upregulating HMGB1 to suppress osteogenic differentiation of bone marrow mesenchymal stem cells.Stem cell research & therapy · 2025Article
- Extracellular vesicles in cardiac surgery: unlocking new frontiers in cardioprotection and patient outcomes.Clinical and experimental medicine · 2025Review
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Controlled Right Ventricular Pressure Overload Can Rescue Left Ventricular Dysfunction by Promoting Biventricular Adaptive Hypertrophy.JACC. Basic to translational science · 2025Article
- Exosomal miR-202-5p derived from iPSC-MSCs protects against myocardial infarction through inhibition of cardiomyocyte pyroptosis.Stem cell research & therapy · 2025Article
- Mesenchymal Stem Cell-Loaded Hydrogel Improves Surgical Treatment for Chronic Cerebral Ischemia.Translational stroke research · 2025Article
- Targeting prominin-2/BACH1/GLS pathway to inhibit oxidative stress-induced ferroptosis of bone mesenchymal stem cells.Stem cell research & therapy · 2025Article
- Inhibition of MALAT1 facilitates ROS accumulation via the Keap1/HO-1 pathway to enhance photodynamic therapy in secondary hyperparathyroidism.Non-coding RNA research · 2025Article
- Extracellular vesicle therapeutics for cardiac repair.Journal of molecular and cellular cardiology · 2025Review
- Multifaceted mechanisms and targeted delivery of mesenchymal stem cell-derived exosomes in cardiovascular diseases: a translational medicine perspective.Frontiers in medicine · 2025Review
- MiR-183-5p inhibitor promotes mitoxantrone-induced immunogenic death of hepatoma cells by targeting STC1.International journal of clinical and experimental pathology · 2025Article
- Exosomes Derived from Apelin-Pretreated Mesenchymal Stem Cells Ameliorate Sepsis-Induced Myocardial Dysfunction by Alleviating Cardiomyocyte Pyroptosis via Delivery of miR-34a-5p.International journal of nanomedicine · 2025Article
- Optimizing therapeutic outcomes: preconditioning strategies for MSC-derived extracellular vesicles.Frontiers in pharmacology · 2025Review
- The Potential of Mesenchymal Stem Cell-Derived Exosomes in Cardiac Repair.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundApplication of mesenchymal stem cell-derived exosomes (MSC-EXO) has emerged as a novel therapeutic strategy for myocardial infarction (MI). Our previous study showed that pretreatment with hemin, a potent heme oxygenase-1 (HO-1) inducer, enhanced the cardioprotective effects of MSCs in a mouse model of MI. This study aimed to investigate the therapeutic effects of EXO derived from hemin-pretreated MSCs (Hemin-MSC-EXO) in MI and explore the potential mechanisms.
methodsMSC-EXO and Hemin-MSC-EXO were collected and characterized. MSC-EXO and Hemin-MSC-EXO were intramuscularly injected into the peri-infarct region in a mouse model of MI. Heart function of mice was assessed by echocardiography. The mitochondrial morphology of neonatal mice cardiomyocytes (NMCMs) under serum deprivation and hypoxic (SD/H) conditions was examined by Mitotracker staining. The cellular senescence of NMCMs was determined by senescence-associated-β-galactosidase assay. A loss-of-function approach was adopted to determine the role of Hemin-MSC-exosomal-miR-183-5p in the regulation of cardiomyocyte senescence
resultsEXO were successfully isolated from the supernatant of MSCs and Hemin-pretreated MSCs. Compared with MSC-EXO, injection of Hemin-MSC-EXO significantly improved cardiac function and reduced fibrosis. Both MSC-EXO and Hemin-MSC-EXO ameliorated cardiomyocyte senescence and mitochondrial fission in vitro and in vivo, and the latter exhibited better protective effects. MicroRNA sequencing revealed a higher level of miR-183-5p in Hemin-MSC-EXO than in MSC-EXO. MiR-183-5p knockdown partially abrogated the protective effects of Hemin-MSC-EXO in attenuating mitochondrial fission and cellular senescence of cardiomyocytes induced by SD/H. High mobility group box-1 (HMGB1) abundance was lower in Hemin-MSC-EXO-treated than MSC-EXO-treated mouse hearts, and HMGB1 was identified as one of the potential target genes of miR-183-5p. Mechanistically, Hemin-MSC-EXO inhibited SD/H-induced cardiomyocyte senescence partially by delivering miR-183-5p into recipient cardiomyocytes via regulation of the HMGB1/ERK pathway. Furthermore, knockdown of miR-183-5p reduced the Hemin-MSC-EXO-mediated cardioprotective effects in a mouse model of MI.
conclusionOur results reveal that Hemin-MSC-EXO are superior to MSC-EXO in treating MI. Exosomal miR-183-5p mediates, at least partially, the cardioprotective effects of Hemin-MSC-EXO by inhibiting cardiomyocyte senescence via regulation of the HMGB1/ERK pathway. This study highlights that MSC-EXO have high translational value in repairing cardiac dysfunction following infarction.
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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.