Tet2 ^ΔMye -induced myeloid hematopoiesis in aging mice accelerate liver fibrosis. (A) A chimeric mouse model of Tet2^ΔMye-induced myeloid hematopoiesis was constructed in young and aged mice. CCl₄ was administered to induce liver fibrosis in young-BMT and old-BMT mice. (B) The profiles the reconstruction of CD45.2⁺Tet2^−/− BMCs in the peripheral blood of young-BMT and old-BMT mice (n = 4 for each group). (C and D) Blood cell composition of CD45.2⁺ cells in young-BMT and old-BMT mice with (C) or without (D) CCl₄-induced liver fibrosis (n = 4 for each group). (E) Frequency of pMDMs in livers of young-BMT and old-BMT mice with CCl₄-induced liver fibrosis (n = 4 for each group). (F) The serum levels of Ccl2, Ccl8, and IL-6 in young-BMT and old-BMT mice with liver fibrosis (n = 4 for each group). (G and H) Picrosirius red staining (G) (scale bar, 125 μm) and statistical analysis (H) of collagen deposition in livers of CCl₄-treated young-BMT and old-BMT mice after Bindarit plus anti–IL-6 Abs treatment (n = 4 for each group). (I and J) Changes in serum Col IV (I) and HA (J) levels in young-BMT and old-BMT mice treated with Bindarit, anti–IL-6 Abs, or Bindarit plus anti–IL-6 Abs. Data are representative of at least two independent experiments with similar results (A–J). All data are shown as mean ± SD and were analyzed by two-tailed, unpaired Student’s t test (C–F), or two-way ANOVA with Sidak’s multiple comparison test (H–J). ***P < 0.001; **P < 0.01; *P < 0.05; P > 0.05 not significant (ns).