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Tregs also highly express immune checkpoint molecules (e.g., CTLA-4, PD-1, GITR), which bind receptors on immune cells to inhibit effector activity [36]

HSCs are converted into myofibroblasts after activation, resulting in excessive deposition of ECM and fibrosis ( The vitamin intervention discussed in this article mainly targets a specific group of people, namely patients with liver fibrosis

Inhibiting CDK1 overcomes oxaliplatin resistance in CRC by regulating acyl-CoA synthetase long-chain family member 4 (ACSL4)-mediated ferroptosis (Zhao et al., 2019)

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without ultrasound guidance