ArticleMolecular therapy. Methods & clinical development2025
Enhanced B cell electroporation efficiency via inhibition of DNA-induced apoptosis and pyroptosis with pan-caspase inhibitor.
Article in Molecular therapy. Methods & clinical development, 2025. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Research Progress of Cuproptosis in Orthopaedics: Opportunities and Challenges.Journal of cellular and molecular medicine · 2026Review
- Engineering delivery platforms for CRISPR-Cas and their applications in healthcare, agriculture and beyond.Nanoscale advances · 2026Review
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Authors and funding
6 authors.
Funding
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Abstract
B cells have immense potential as gene therapy carriers because of their ability to secrete therapeutic proteins and mediate immunological memory and tolerogenic functions. However, efficient gene delivery into primary B cells remains a challenge, as DNA electroporation frequently induces significant cell death. Here, we demonstrate that primary murine B cells undergo apoptosis and pyroptosis after DNA electroporation, which is driven primarily by activation of the cyclic GMP-AMP synthase stimulator of interferon genes (cGAS-STING) pathway in response to cytoplasmic double-stranded DNA (dsDNA). To overcome this, we pretreated B cells with a caspase inhibitor, which increased cell viability and improved DNA delivery and knock-in efficiency. Notably, compared with the inhibition of either apoptosis or pyroptosis alone, treatment with the pan-caspase inhibitor Boc-D-FMK resulted in a more significant improvement in cell viability and DNA electroporation efficiency. This approach significantly increased the expression and secretion of human erythropoietin (hEPO) both
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