Table 2.
Biological impacts caused by different carbon nanomaterials (CNMs) via various signaling pathways.
| Type of CNM | Model System | Receptor/Key Mediator | Signaling Pathways | Biological Impact | Ref. |
|---|---|---|---|---|---|
| Graphene | |||||
| Graphene oxide nanosheets | Macrophage cell RAW264.7 | TLR4, TLR9 | MyD88, TRAF6, NF-κB | Autophagy of macrophages; Inflammation | [129] |
| Graphene oxide nanoribbons non-covalently functionalized with PEG-DSPE (O-GNR-PEG-DSPE) | 11 different malignant human cell lines | EGFRs | JAK/STAT; MAPK/ERK (Ras/Raf/MEK/ERK) |
Cell proliferation | [130] |
| Printex 90 (Carbon black) | Rat lung epithelial cells | EGFR | MAPK/ERK (Ras/Raf/MEK/ERK) | Cell proliferation | [131,132,133] |
| β1-integrin | Cell adhesion; Angiogenesis; Migration | ||||
| Fullerene | |||||
| Fullerenol-1 (13-15 hydroxyl substituents) | A7r5 cells (rat aortic smooth muscle cells, human coronary artery smooth muscle cells | PTK | Protein kinase C | Antiproliferative effect | [134] |
| Fullerenol 24 hydroxyl substituents) | Human lung cells (type II alveolar epithelial A549) | No data | p38 MAPK | Nrf2-induced antioxidative defense | [135] |
| Carbon Nanotubes | |||||
| Long CNT | Met5a mesothelial cells; THP-1 macrophages | TLRs; P2X7 | NF-κB; STAT-1; MAPK; RTK | Inflammation and fibrosis in lungs | [136,137,138] |
| SWCNTs | Human mesothelial cells | EGF; PDGF | NF-κB, AP-1, and MAPK (ERK, p38) | ROS-induced inflammation; Apoptosis | [139] |
| SWCNTs | Human lung fibroblast (WI-38-VA13) | TGFβ; PDGF | NF-κB | ROS-induced inflammation; Fibroblast-to- myofibroblast transformation |
[140] |
| SWCNTs | Human lung fibroblasts | TGFβ; VEGF | p38 MAPK | Fibroproliferation Angiogenesis | [141] |
| MWCNT | Mouse macrophages (RAW264.7) | NF-κBp65 | NF-κB | Inflammation | [140] |
| MWCNTs | Human lung fibroblasts (WI38-VA13) | TGFβ; PDGF | NF-κB | Fibroblast-to- myofibroblast transformation |
[140] |
| MWCNTs | Human bronchial epithelial cell line (BEAS–2 B) | ERK1; p38; HSP27 | MAPK/ERK | Cell proliferation; Cell adhesion | [142] |
| Carbon Dots | |||||
| CDs | Yeast cells (Pichia pastoris) | No data | No data | ROS response: Growth inhibition |
[143] |
| Pristine CDs (negative charge) | Mouse fibroblasts (NIH/3T3) | No data | No data | ROS response; Arrest of the G2/M phase | [58] |
| Polyethylenimine-coated CDs (positive charge) | Mouse fibroblasts (NIH/3T3) | No data | No data | Disruption of G0/G1 phase of cell cycle | [58] |
| Graphene CDs | HUEVEC cells | O2 | Energy-transfer/Electron-transfer pathways | ROS response | [144] |
| Graphene CDs | THP-1-activated macrophages | Bcl2, Bax, Bad | p38 MAPK; NF-κB | Apoptosis | [145] |
| Beclin 1; LC3 | Autophagy | ||||
| NF-κBp65 | ROS-induced Inflammation | ||||
| Nanodiamonds | |||||
| NDs | Monoblastoid cells (U937) | TLR4 | NF-κB | Apoptosis; Inflammation |
[146] |
| NDs | Alzheimer’s Disease Rat Model | NMDA receptors | NF-κB; STAT3 | Neuroprotection—inhibition of Inflammation; Antioxidative defense |
[147] |
| NDs | Human peripheral lymphocytes | O− | No data | Apoptosis; Oxidative stress |
[110] |