Renal tubular-derived retinoic acid drives renal fibrosis via a RAI14–TRIOBP–YAP mechanotransduction axis

doi:10.1016/j.cellsig.2025.112246

Renal tubular-derived retinoic acid drives renal fibrosis via a RAI14–TRIOBP–YAP mechanotransduction axis

2025-11-14

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DOI：10.1016/j.cellsig.2025.112246

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• Identifies injured tubules as a source of paracrine retinoic acid (RA) that drives renal fibrosis. • Reveals RAI14 as a crucial RA-induced effector essential for fibroblast activation. • Elucidates a mechanotransduction mechanism where RAI14 stabilizes TRIOBP to enhance F-actin assembly and cytoskeletal tension. • Establishes the complete RA–RAI14–TRIOBP–YAP axis linking metabolic signaling to profibrotic transcriptional reprogramming.

Renal tubular-derived retinoic acid drives renal fibrosis via a RAI14–TRIOBP–YAP mechanotransduction axis

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