General Information of the Disease (ID: DIS00107)
Name
Periodontitis
ICD
ICD-11: DA0C
Full List of Target(s) of This Ferroptosis-centered Disease
Transferrin receptor protein 1 (TFRC)
In total 2 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Marker/Suppressor/Driver
Responsed Disease Periodontitis [ICD-11: DA0C]
Responsed Regulator LINC00616 (IncRNA) Driver
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model hPLSCs (Periodontal ligament stem cells)
Response regulation Inhibition of LINC00616 promoted cell viability and suppressed ferroptosis of PDLSCs. miR-370 was verified to be a target of LINC00616. Additionally, miR-370 targeting the transferrin receptor protein and upregulated transferrin receptor (TFRC) abolished the effects of overexpressed miR-370 on cell viability and ferroptosis of PDLSCs. Therefore, LINC00616 knockdown may be a promising therapeutic strategy for periodontitis.
Experiment 2 Reporting the Ferroptosis-centered Disease Response by This Target [1]
Target for Ferroptosis Marker/Suppressor/Driver
Responsed Disease Periodontitis [ICD-11: DA0C]
Responsed Regulator hsa-miR-370-3p (miRNA) Suppressor
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model hPLSCs (Periodontal ligament stem cells)
Response regulation Inhibition of LINC00616 promoted cell viability and suppressed ferroptosis of PDLSCs. miR-370 was verified to be a target of LINC00616. Additionally, miR-370 targeting the transferrin receptor protein and upregulated transferrin receptor (TFRC) abolished the effects of overexpressed miR-370 on cell viability and ferroptosis of PDLSCs. Therefore, LINC00616 knockdown may be a promising therapeutic strategy for periodontitis.
Nuclear receptor coactivator 4 (NCOA4)
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis-centered Disease Response by This Target [2]
Target for Ferroptosis Driver
Responsed Disease Periodontitis [ICD-11: DA0C]
Responsed Drug Butyrate Investigative
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model hPDLFs (Human periodontal ligament fibroblasts)
Response regulation Periodontitis-level butyrate disrupted iron homeostasis by activation of NCOA4-mediated ferritinophagy, leading to ferroptosis in PDLFs. Butyrate-induced iron accumulation, reactive oxygen species (ROS) generation, glutathione depletion and lipid peroxidation in PDLFs, and the butyrate-induced ferroptosis can be blocked by the lipid peroxide scavenger ferrostatin-1.
References
Ref 1 Long non-coding RNA LINC00616 promotes ferroptosis of periodontal ligament stem cells via the microRNA-370 / transferrin receptor axis. Bioengineered. 2022 May;13(5):13070-13081. doi: 10.1080/21655979.2022.2076508.
Ref 2 Periodontitis-level butyrate-induced ferroptosis in periodontal ligament fibroblasts by activation of ferritinophagy. Cell Death Discov. 2020 Nov 10;6(1):119. doi: 10.1038/s41420-020-00356-1.