Fibroblast activation protein-targeted chimeric antigen-receptor-modified NK cells alleviate cardiac fibrosis
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View abstract on PubMed
Summary
This summary is machine-generated.Engineered CAR natural killer (NK) cells targeting fibroblast activation protein (FAP) effectively reduced cardiac fibrosis in mice. This novel therapy shows promise for treating cardiovascular diseases by eliminating FAP-positive cells and improving heart function.
Area Of Science
- Immunotherapy
- Cardiovascular Research
- Cell Biology
Background
- Cardiac fibrosis (CF) is a key factor in cardiovascular disease progression, involving myofibroblast transdifferentiation.
- Fibroblast activation protein (FAP) is a specific marker for activated myofibroblasts.
- Chimeric antigen receptor (CAR)-based therapy offers a promising immunotherapy approach.
Purpose Of The Study
- To construct CAR natural killer (NK) cells targeting FAP for potential CF therapy.
- To evaluate the efficacy and mechanism of FAP-targeted CAR-NK cells in preclinical models of cardiac fibrosis.
Main Methods
- Development of FAP-specific CAR-NK-92 cells.
- In vitro assessment of FAP CAR-NK cell cytotoxicity, cytokine secretion, and degranulation against FAP+ cells and cardiac fibroblasts.
- In vivo studies using a mouse model of Ang II/PE-induced cardiac injury.
Main Results
- FAP CAR-NK-92 cells specifically recognized and killed FAP+ cells in vitro.
- Enhanced cytotoxicity, cytokine secretion, and degranulation of FAP CAR-NK cells compared to parental NK-92 cells.
- In vivo administration of FAP CAR-NK cells improved cardiac function and reduced fibrosis, with evidence of increased apoptosis in target cells.
Conclusions
- FAP CAR-NK-92 cells demonstrate specific targeting and potent anti-fibrotic effects in vitro and in vivo.
- This CAR-NK cell-based therapy represents a potential therapeutic strategy for cardiac fibrosis patients.
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