Disease Information
General Information of the Disease (ID: DIS00310)
| Name |
Idiopathic interstitial pneumonitis
|
|---|---|
| ICD |
ICD-11: CB03
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| Resistance Map |
Type(s) of Resistant Mechanism of This Disease
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Key Molecule: Long non-protein coding RNA (CHRF) | [1] | |||
| Resistant Disease | Pulmonary fibrosis [ICD-11: CB03.1] | |||
| Molecule Alteration | Up-regulation | Interaction |
||
| Resistant Drug | Silicon dioxide | |||
| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vitro Model | THP-1 cells | Blood | Homo sapiens (Human) | CVCL_0006 |
| MRC-5 cells | Lung | Homo sapiens (Human) | CVCL_0440 | |
| RAW 264.7 cells | Ascites | Mus musculus (Mouse) | CVCL_0493 | |
| NIH/3T3 cells | Whole embryo | Mus musculus (Mouse) | CVCL_0594 | |
| In Vivo Model | Pulmonary fibrosis miR-489 overexpression mouse model | Mus musculus | ||
| Experiment for Molecule Alteration |
Overexpression assay | |||
| Experiment for Drug Resistance |
Immunofluorescence assay | |||
| Mechanism Description | CHRF-miR-489-MyD88 Smad3 signaling axis exerts key functions in silica-induced pulmonary fibrosis and may represent a therapeutic target for silicosis. | |||
Investigative Drug(s)
1 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Key Molecule: SIRT1 antisense RNA (SIRT1-AS) | [2] | |||
| Resistant Disease | Pulmonary fibrosis [ICD-11: CB03.1] | |||
| Molecule Alteration | Down-regulation | Expression |
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| Resistant Drug | Astragaloside IV | |||
| Experimental Note | Discovered Using In-vivo Testing Model | |||
| In Vitro Model | RLE-6TN cells | Lung | Rattus norvegicus (Rat) | CVCL_4693 |
| Experiment for Molecule Alteration |
Overexpression assay; Knockdown assay | |||
| Experiment for Drug Resistance |
CCK8 assay | |||
| Mechanism Description | Collectively, sirt1 AS was critical for ASV-mediated inhibition of IPF progression and targeting of sirt1 AS by ASV could be a potential therapeutic approach for IPF. | |||
References
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