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Fibronectin extra-domain A (EDA), also known as EIIIA, is an alternatively spliced segment of the fibronectin (FN) protein. It is upregulated during tissue injury, wound healing, fibrosis, chronic inflammation, atherosclerosis, and cancer progression. EDA-FN modulates matrix assembly and cell signaling, and its expression is associated with disease severity in asthma, fibrosis, and cancer, making it a therapeutic target. EDA interacts with TLR4 to promote inflammatory gene expression. Therapies targeting EDA-FN are being developed.
Therapeutic strategies include CAR-T cell therapy targeting EDA-FN in tumors, aiming to eliminate cancer cells expressing this isoform in the ECM.
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