Table 4.
CRISPR/Cas9 for cartilage repair.
| Target gene | Repair Mechanism | Research progress | Literature |
|---|---|---|---|
| DANCR | Activation of DANCR significantly promotes the differentiation of adipose stem cells to chondrocytes and enhances cartilage formation in vitro. Upregulation | Packaged dCas9-VPR and its corresponding gRNA into a baculovirus for gene transfection and compared four dCas9-VPRs derived from different bacteria, showing that SadCas9-VPR derived from Staphylococcus aureus successfully induced DANCR activation in rat adipose stem cells. | Nguyen et al., [102] 2021 |
| MMP13 | Reduction of total MMP13 secretion by CRISPR/Cas9 indirectly reduces degradation of the extracellular matrix. Knock-down. | Reconstructed human articular chondrocyte populations using a CRISPR/Cas9-mediated gene editing strategy that stably reduced MMP13 expression in cartilage. | Seidl et al., [103] 2019 |
| ACAN and Col2 | As a major component of the ECM, collagen not only provides mechanical support but also controls the growth and differentiation of cells. Upregulation. | Used the dCas-VPR CRISPR gene activation system to upregulate aggrecan (ACAN) and Col2. | Farhang et al., [104] 2020 |
| TRPV4 | A mutation in TRPV 4 is a functional mutation that can lead to an increase in intracellular calcium ion levels. Repair template. | In the presence of TRPV 4-specific agonists, the mutant group showed significantly accelerated cartilage differentiation at early stages and upregulated Sox9 mRNA expression. | Nonaka et al., [106] 2019 |
| Cx43 | High levels of transmembrane protein Cx43 expression in osteoarthritic cartilage. Cx43 also upregulated p16INK4a and NF-κB to cause senescence and apoptosis in chondrocytes. Knock-down. | Used CRSIPR/Cas9 to downregulate Cx43 expression and successfully slowed cartilage degeneration. | Varela-Eirín et al., [109] 2018 |
| COL2A1-GFP | Purification by identifying surface markers would greatly improve chondrogenic efficiency. Knock-in. | The CD146+/CD166+/PDGFRβ+/CD45- subpopulation of chondrogenic progenitor cells possessed more powerful chondrogenic ability. | Dicks et al., [117] 2020 |