ArticleFrontiers in cell and developmental biology2021
Apelin Rejuvenates Aged Human Mesenchymal Stem Cells by Regulating Autophagy and Improves Cardiac Protection After Infarction.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Rejuvenation of Bone Marrow Mesenchymal Stem Cells: Mechanisms and Their Application in Senile Osteoporosis Treatment.Biomolecules · 2025Pooled it
- International Union of Basic and Clinical Pharmacology. CXXI. Apelin receptor pharmacology in the human cardiovascular system and emerging clinical applications.Pharmacological reviews · 2026Review
- Circulating apelin levels fail to link sarcopenia-related muscle parameters in older adults.The journal of nutrition, health & aging · 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
- Genetically modified mesenchymal stromal cells: a cell-based therapy offering more efficient repair after myocardial infarction.Stem cell research & therapy · 2024Review
- Pharmacokinetic characteristics of mesenchymal stem cells in translational challenges.Signal transduction and targeted therapy · 2024Review
- Mechanisms of Myocardial Edema Development in CVD Pathophysiology.Biomedicines · 2024Review
- Engineering mesenchymal stem cells for premature ovarian failure: overcoming challenges and innovating therapeutic strategies.Theranostics · 2024Review
- mTOR signalling pathway in stem cell bioactivities and angiogenesis potential.Cell proliferation · 2023Review
- TRAF3IP2 drives mesenchymal stem cell senescence via regulation of NAMPT-mediated NAD biosynthesis.Heliyon · 2023Article
- Adipokines at the crossroads of obesity and mesenchymal stem cell therapy.Experimental & molecular medicine · 2023Review
- Cardiac and intestinal tissue conduct developmental and reparative processes in response to lymphangiocrine signaling.Frontiers in cell and developmental biology · 2023Review
- Apelin-13 Pretreatment Promotes the Cardioprotective Effect of Mesenchymal Stem Cells against Myocardial Infarction by Improving Their Survival.Stem cells international · 2022Article
- Tumorigenic Aspects of MSC Senescence-Implication in Cancer Development and Therapy.Journal of personalized medicine · 2021Review
- Hypoxic preconditioning rejuvenates mesenchymal stem cells and enhances neuroprotection following intracerebral hemorrhage via the miR-326-mediated autophagy.Stem cell research & therapy · 2021Article
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The protective effects of mesenchymal stem cell (MSC)-based therapy for myocardial infarction (MI) are largely hampered as they age. Apelin is an endogenous ligand of its receptor APJ and plays an essential role in regulating multiple biological activities including MSC proliferation and survival. In this study, we investigated whether Apelin regulates MSC senescence and whether its overexpression could rejuvenate aged MSCs (AMSCs) to improve cardiac protection following infarction in mice. MSC senescence was evaluated by senescence-associated β-galactosidase assays. Apelin level was examined by western blotting. Autophagy was determined by transmission electron microscopy. The cardioprotective effect of AMSCs with Apelin overexpression (Apelin-AMSCs) was assessed in a mouse MI model. Apelin expression was dramatically reduced in AMSCs. Interestingly, knockdown of Apelin induced young MSCs (YMSC) senescence, whereas overexpression rescued AMSC senescence. Apelin overexpression also increased AMSC angiogenic capacity. Mechanistically, Apelin overexpression upregulated the autophagy level of AMSCs by activating AMP-activated protein kinase (AMPK) signaling, thereby rejuvenating AMSCs. Compared with AMSCs, transplantation of Apelin-AMSCs achieved better therapeutic efficacy for MI by enhancing cell survival and angiogenesis. In conclusion, our results reveal that Apelin activates AMPK to rejuvenate AMSCs by increasing autophagy and promotes cardioprotection following infarction in mice. This study identified a novel target to rejuvenate AMSCs and enhance their therapeutic efficacy.
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