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Updated: Jan 10, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Direct cell reprogramming by a designed agonist inducing HER2-FGFR proximity.

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    This summary is machine-generated.

    Synthetic ligands called Novokines can reprogram cell identity by forcing receptor pairs together. One Novokine, H2F, reprograms fibroblasts into muscle cells, showing promise for regenerative medicine.

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    Area of Science:

    • Cell biology
    • Biochemistry
    • Regenerative medicine

    Background:

    • Growth factor signaling pathways control cell fate.
    • Receptor dimerization and activation are key to these pathways.
    • Targeting novel receptor pairs offers a way to engineer cell identity.

    Purpose of the Study:

    • To investigate de novo designed synthetic ligands (Novokines) for cell reprogramming.
    • To explore the potential of inducing proximity between novel receptor pairs, specifically HER2 and FGF receptor.
    • To assess the therapeutic capacity of engineered receptor signaling for cell fate engineering and regeneration.

    Main Methods:

    • De novo design of synthetic ligands (Novokines).
    • Utilizing FRET assays to confirm receptor proximity.
    • Employing phosphoproteomic analysis to identify downstream signaling.
    • Assessing myogenic differentiation and myofiber formation in vitro.

    Main Results:

    • A synthetic ligand, H2F, successfully induced proximity between HER2 and FGF receptor.
    • H2F demonstrated potent signaling activity, reprogramming fibroblasts into myogenic cells.
    • H2F selectively activated the MAPK pathway, bypassing PLCγ-mediated Ca²⁺ signaling.
    • H2F treatment promoted significant myofiber formation from patient-derived myoblasts.

    Conclusions:

    • Synthetic receptor pairings can be designed to rewire cellular signaling outputs.
    • Novokines offer a programmable platform for cell fate engineering.
    • Engineered receptor interactions can drive regeneration, with potential applications in therapeutic myogenesis.