ArticleJournal of advanced research2026
Asprosin-driven metabolic-epigenetic rewiring attenuates mesenchymal stem cell senescence with therapeutic benefits for infarcted hearts.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Mesenchymal Stromal Cell Rejuvenation Strategies to Enhance Clinical Translation in Cell Therapy.Aging cell · 2026Review
- Lactylation in cardiac repair: Nexus and therapeutic opportunity.Journal of molecular and cellular cardiology plus · 2026Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionSenescent mesenchymal stem cells (MSCs) exhibit impaired self-renewal, limiting their therapeutic potential. While multi-omics have revealed downregulation of pan-tissue Fbn1 with aging, particularly in MSCs, the role of its derivative asprosin in MSC senescence is unknown.
objectivesTo elucidate the regulation of senescence/reparative function in aged MSCs by asprosin and evaluate its therapeutic potential for aged MSC-mediated cardiac repair after myocardial infarction (MI).
methodsSerum asprosin levels were measured by enzyme-linked immunosorbent assay, and asprosin expression in MSCs was determined by western blotting. Fbn1 expressiondynamics with aging were assessed using public transcriptomic/single-cell datasets. Gain/loss-of-function (lentiviral overexpression/CRISPR-Cas9 knockout) studies were employed to validate the role of asprosin. The effects of recombinant asprosin on senescent MSC proliferation, migration, and pro-angiogenic secretion were tested. Glycolytic flux (Seahorse), metabolites (glucose uptake, G-6-P, lactate), and lactylation (pan-lysine, H3K18la) were measured. Integrated H3K18la CUT&Tag/RNA-seq was performed to identify downstreamtargets, and therapeutic efficacy was assessed in an MI mouse model using intramyocardial injection of asprosin-overexpressing aged MSCs.
resultsCirculating asprosin was correlated with adipose mass in young obese mice but was attenuated in aged obese mice. Consistently, human cohorts (normal body mass index) showed an inverse age-asprosin correlation. Systemic and MSC-specific asprosin expression significantly declined with aging. Asprosin knockout intensified H
conclusionAsprosin is a novel MSC-specific rejuvenation factor that antagonizes senescence through metabolic-epigenetic interplay. Targeting the asprosin-driven "Glycolysis-Lactylation-Epigenetics" axis offers a transformative strategy to enhance MSC-based therapies for ischemic heart disease.
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