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Interfering with this pathway, either by disrupting the core regulator CLOCK:BMAL1 or activating the nuclear receptors REV-ERBs, significantly reduced HSC activation. We also identified transgelin as the downstream effector of clock-regulated HSC contractility, a characteristic of HSC activation. Transgelin is regulated indirectly by a BMAL1-CK1\u03b5 signaling pathway and directly by REV-ERB\u03b1. Our findings identify a hitherto undescribed mechanism that links the molecular clock to HSC activation and cell contractile function, which is relevant to human fibrotic diseases. This pathway provides several entry points for drugs to target and disrupt primary fibrogenic signaling. 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