Table 2 Therapeutic targets for RCD in osteoporosis and periodontitis.
Drugs | Mechanism for the treatment of osteoporosis | RCD | Drugs | Mechanism for the treatment of periodontitis |
|---|---|---|---|---|
COX19, MAP-2K2, FDX1 | Strongly correlated with immune cell infiltration and associated with osteoporosis prognosis. | Cuproptosis | ME-344, NV-128, RILUZOLE | Demonstrated good affinity for target genes(SLC7A11, SLC3A-2, RPN1, NCKAP1, LRPPRC, NDUFS1). |
TXNRD1 inhibitors | Increases bone cystine content, reduces osteoclast numbers, and mitigates bone loss. | disulfidptosis | Target molecules | MLKL, DCN, IL1B, and IL18. Reduce inflammation and tissue destruction. |
PGRMC2 | Modulates the differentiation of monocytes into macrophages and influences BM-MSC behavior. | disulfidptosis | ZBP1 Inhibitor | Reduces inflammatory cytokine secretion and cell death. |
BMDMs | Essential cells in macrophage activation and osteolysis. | PANoptosis | Caspase-1 Inhibitor | Alleviate inflammation and tissue damage. |
Apelin-13 | Regulates autophagy, apoptosis, and inflammation, exerting multifaceted protective effects on bone. | PANoptosis | RIPK1/3 Blockor | Prevents necroptotic cell death and subsequent inflammation. |
| Â | Â | PANoptosis | CEBPG, TFA-P2C, BNIP3 | Tissue biomarkers for periodontitis. |
| Â | Â | PANoptosis | TTM | Promotes autophagosome formation and enhances mitophagy-related gene expression, while counteracting LPS-induced suppression of autophagic flux. Mitigates LPS-induced lysosomal dysfunction. Increases lysosomal membrane permeability and the secretion of cathepsin B. Enhances autophagic flux and lowers cathepsin B levels. |
