International journal of pharmaceuticsJul 16, 2026

Stem cell membrane-coated nanoparticles may reduce heart scarring by restoring energy balance in heart cells

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 17, 2026

Abstract

MM@NPs/Mdivi-1 significantly improved cardiac function and reduced collagen deposition in a murine cardiac fibrosis model.

Myocardial fibrosis is linked to heart failure and may be driven by excessive mitochondrial fission.
Mdivi-1, a Drp1 inhibitor, faces challenges with solubility and cardiac targeting.
A novel delivery system using mesenchymal stem cell membranes effectively enhances Mdivi-1's cellular uptake in damaged heart cells.
In vitro results showed that the new system restored mitochondrial integrity and suppressed damaging cellular signals.
In a mouse model of cardiac fibrosis, the treatment improved heart function and reduced fibrotic tissue formation.
The anti-fibrotic effects could be related to the activation of a specific cellular recycling process.

Simplified

Myocardial fibrosis is a critical pathological endpoint in heart failure, yet effective targeted therapies remain lacking. Dysregulation of mitochondrial dynamics, particularly Drp1-mediated excessive fission, drives cardiomyocyte dysfunction and pro-fibrotic signaling. Mdivi-1 is a selective Drp1 inhibitor, but suffers from poor solubility, lack of cardiac targeting, and potential systemic toxicity. To address these limitations, we developed a mesenchymal stem cell membrane-coated biomimetic nanodelivery system (MM@NPs/Mdivi-1) with high drug loading capacity and pH-responsive release properties. In vitro, MM@NPs/Mdivi-1 enhanced cellular uptake in injured cardiomyocytes, restored mitochondrial network integrity and membrane potential, and suppressed Drp1 phosphorylation. In an isoproterenol-induced murine cardiac fibrosis model, the system achieved cardiac-specific enrichment, improved cardiac function, reduced collagen deposition, and restored mitochondrial ultrastructure. Mechanistically, transcriptomics combined with functional rescue experiments revealed that its anti-fibrotic effects were dependent on FUNDC1-mediated mitophagy activation. Collectively, MM@NPs/Mdivi-1 effectively attenuates myocardial fibrosis by restoring mitochondrial homeostasis, offering a promising targeted nanotherapeutic strategy for heart failure.

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Funding

Competing interests

No financial or personal ties reported.

PubMed

Stem cell membrane-coated nanoparticles may reduce heart scarring by restoring energy balance in heart cells

Abstract

Full Text

Funding

Competing interests

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