Table 3 NM-induced injuries that contribute to fibrosis

Si-NPs

64.43 ± 10.50 nm

ICR mice

20 mg/kg b.w., 15 d, intravenous injection

Induced hepatic damage, fibrosis, and TGF-β1/SMAD3 signaling activation

[6]

TiO₂-NPs

21 nm

Rats

0.5, 1.5, 5, 15, 50, and 150 mg/kg b.w.; intratracheal instillation, 1 month

Induced hepatic profibrotic alterations

[57]

TiO₂-NPs

5–6 nm

ICR mice

2.5, 5, and 10 mg/kg b.w.; oral administration, 9 months

Triggered hepatic fibrosis and upregulated expression of TGF-β/SMAD/MAPK/WNT pathway-related factors

[58]

Cu-NPs

32.7 ± 10.45 nm

SD rats

100, 200, or 400 mg/kg b.w./day; 28 d, oral administration,

Induced early hepatic fibrotic changes via TGF-β/SMAD signaling

[60]

Ag-NPs

56 nm

SD rats

30, 125, 500 mg/kg b.w., oral exposure, 13 w

Triggered fibrosis in the bile duct

[63]

TiO₂-NPs

6.5 nm

ICR mice

2.5, 5, 10 mg/kg b.w.; nasal exposure, 9 months

Induced pulmonary toxicity involving reactive free radical-activated TGF-β/SMAD/P38MAPK/WNT signaling

[66]

NiO-NPs

44 nm

Wistar rats, HepG2 cells

0.015–0.24 mg/kg, 9 w, intratracheal instillation

Induced elevated levels of types I and III collagen in the liver and proteins involved in TGF-β1-mediated SMAD pathway

[64]

MWCNTs, SWCNTs, Carbon black

CNTs: 0.3–49 nm × 0.5–10 μm, Silica: 1.6 μm Black carbon: 14 nm

J774A macrophages

2.5 μg/mL, 24 h

MWCNTs and SWCNTs stimulated myofibroblast transformation of macrophages

[201]