Fig. 8. TASCCs are also observed in human kidney diseases.

(A) Coimmunostaining of mTOR and LC3 in biopsies of human control nonfibrotic and fibrotic kidneys [controls (n = 5); AKI (n = 10); chronic interstitial nephritis (Chronic IN) (n = 10); AAN (n = 10); and DKD (n = 10)]. Control tissues are normal-appearing renal peritumoral tissues. Arrows mark TASCCs. (B) Quantification of TASCC⁺ tubular cells per field (×40). (C) Colocalization of pH3 and mTOR in human kidney biopsies with fibrosis (n = 10 per group) and controls (n = 5). Scale bars, 10 μm. (D) Quantification of pH3⁺ tubular cells with TASCC per field (40×). Arrows, pH3⁺ nuclei. Data are means ± SEM. ANOVA–Tukey’s post hoc test. ***P < 0.001, controls versus kidney with fibrosis. (E) This cartoon summarizes the involvement of CG1, TASCC, cell cycle, and senescence in the development of fibrosis. Severe kidney injury results in substantial DNA damage, leading to activation of CG1 that suppresses G₂-M transition. G₂-M arrest triggers a senescence-like state, initiating the formation of the TASCC organelle, and a TASCC-induced pro-secretory phenotype. Prolonged CG1 expression and the resulting G₂-M arrest and TASCC-induced secretion promotes fibrosis.