A systematic review and meta-analysis evaluated the efficacy of emodin in animal models of pulmonary fibrosis and its molecular mechanisms. Emodin significantly reduced the severity of fibrosis by several measures, such as Ashcroft score (SMD = -3.10; 95% CI: -4.40 to -1.79) and fibrotic area (SMD = -4.97; 95% CI: -7.87 to -2.08). It also reduced hydroxyproline content (SMD = -1.91; 95% CI: -2.42 to -1.41) and collagen deposition, while improving markers of lung inflammation (alveolitis; SMD = -1.89; 95% CI: -2.21 to -1.57) and pulmonary coefficients. Emodin reduced inflammation by reducing the levels of inflammatory cytokines IL-6 (SMD = -3.86; 95% CI: -6.21 to -1.51), IL-1β (SMD = -3.21; 95% CI: -4.90 to -1.53) and TNF-α (SMD = -3.31; 95% CI: -3.96 to -2.67). It also reduced oxidative stress by increasing the activity of the antioxidant enzyme SOD (SMD = 4.69; 95% CI: 3.59 to 5.80) and decreasing MDA levels (SMD = -3.58; 95% CI: -4.48 to -2.68). In addition, emodin inhibited epithelial-mesenchymal transition (EMT) and reduced TGF-β1 levels (SMD = -2.68; 95% CI: -3.41 to -2.02). The authors state that some of the differences between studies were related to different dosing schedules and animal species used, and recommend further investigation into the antifibrotic properties of emodin.