ArticleAging cell2020
miR-155-5p inhibition rejuvenates aged mesenchymal stem cells and enhances cardioprotection following infarction.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 110 citations in OpenAlex.
- The Yin and Yang of cellular senescence in ischemia-induced myocardial injury.Trends in cardiovascular medicine · 2026Review
- Exercise rejuvenates bone marrow mesenchymal stem cells associated with the inhibition of inflammatory factors and senescence-related factors.Biochemistry and biophysics reports · 2026Article
- Crosstalk between lipid metabolism and epigenetics in cellular senescence and age-related diseases.npj aging · 2026Review
- Epigenetic H3K4me3 activation of miR-155-5p promotes intervertebral disc degeneration via autophagy and ageing in nucleus pulposus cells.Non-coding RNA research · 2026Article
- Cancer and aging: complex associations and therapeutic targets.Molecular biomedicine · 2026Review
- Hematopoietic (stem) cells-The elixir of life?FEBS letters · 2026Review
- Interpretation of the molecular mechanism and therapeutic potential of microRNA‑155 in cardiovascular and cerebrovascular diseases (Review).International journal of molecular medicine · 2026Review
- Shared molecular mechanisms in aging and neurodegenerative diseases: from mechanistic insights to therapeutic strategies.Frontiers in human neuroscience · 2026Review
- Intertwined roles of microRNA-155 and metformin in osteoarthritis: Novel potential diagnostic, prognostic, and therapeutic modulators.World journal of orthopedics · 2025Review
- Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025Review
- Harnessing miRNA therapeutics: a novel approach to combat heart and brain infarctions in atherosclerosis.Cell death discovery · 2025Review
- Earthing effects on mitochondrial function: ATP production and ROS generation.FEBS open bio · 2025Article
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- Sex-Specific Cardiovascular Protection in Developing Metabolic Syndrome: The Role of AMPK.Antioxidants (Basel, Switzerland) · 2025Article
- Unraveling the Complex Cellular Repair Mechanisms Following Myocardial Infarction.International journal of molecular sciences · 2025Review
- Critical analysis of descriptive microRNA data in the translational research on cardioprotection and cardiac repair: lost in the complexity of bioinformatics.Basic research in cardiology · 2025Review
- The influence of cell source on the senescence of human mesenchymal stem/stromal cells.Human cell · 2025Review
- Inhibition of mir-155-5p alleviates cardiomyocyte pyroptosis induced by hypoxia/reoxygenation via targeting SIRT1-mediated activation of the NLRP3 inflammasome.Journal of cardiothoracic surgery · 2025Article
- Mesenchymal Stem Cells Senescence: Mechanism and Rejuvenation Interventions.International journal of medical sciences · 2025Review
- Cartilage-targeting peptide-modified cerium oxide nanoparticles alleviate oxidative stress and cartilage damage in osteoarthritis.Journal of nanobiotechnology · 2024Article
16 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging impairs the functions of human mesenchymal stem cells (MSCs), thereby severely reducing their beneficial effects on myocardial infarction (MI). MicroRNAs (miRNAs) play crucial roles in regulating the senescence of MSCs; however, the underlying mechanisms remain unclear. Here, we investigated the significance of miR-155-5p in regulating MSC senescence and whether inhibition of miR-155-5p could rejuvenate aged MSCs (AMSCs) to enhance their therapeutic efficacy for MI. Young MSCs (YMSCs) and AMSCs were isolated from young and aged donors, respectively. The cellular senescence of MSCs was evaluated by senescence-associated β-galactosidase (SA-β-gal) staining. Compared with YMSCs, AMSCs exhibited increased cellular senescence as evidenced by increased SA-β-gal activity and decreased proliferative capacity and paracrine effects. The expression of miR-155-5p was much higher in both serum and MSCs from aged donors than young donors. Upregulation of miR-155-5p in YMSCs led to increased cellular senescence, whereas downregulation of miR-155-5p decreased AMSC senescence. Mechanistically, miR-155-5p inhibited mitochondrial fission and increased mitochondrial fusion in MSCs via the AMPK signaling pathway, thereby resulting in cellular senescence by repressing the expression of Cab39. These effects were partially reversed by treatment with AMPK activator or mitofusin2-specific siRNA (Mfn2-siRNA). By enhancing angiogenesis and promoting cell survival, transplantation of anti-miR-155-5p-AMSCs led to improved cardiac function in an aged mouse model of MI compared with transplantation of AMSCs. In summary, our study shows that miR-155-5p mediates MSC senescence by regulating the Cab39/AMPK signaling pathway and miR-155-5p is a novel target to rejuvenate AMSCs and enhance their cardioprotective effects.
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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.