General Information of the Disease (ID: M6ADIS0025)
Name
Urinary/pelvic organs injury
ICD
ICD-11: NB92
Full List of Target Gene(s) of This m6A-centered Disease Response
Cytochrome P450 1B1 (CYP1B1)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, transcription factor activating enhancer binding protein 2-alpha (tfap2a), Cytochrome P450 1B1 (CYP1B1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development.
Responsed Disease Injury of kidney [ICD-11: NB92.0]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell apoptosis
In-vitro Model NRK-52E Normal Rattus norvegicus CVCL_0468
In-vivo Model Rats were anesthetized and incised through the midline of the abdomen, and the left renal vertebral arch and arteries were blocked for 45 min, thereby resulting in left kidney ischemia. At the same time, the right kidney was removed, further aggravating the degree of left kidney injury.
Forkhead box protein D1 (FOXD1)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 contributes to renal ischemia-reperfusion injury by regulating Forkhead box protein D1 (FOXD1) methylation. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, transcription factor activating enhancer binding protein 2-alpha (tfap2a), cytochrome P-450 1B1 (cyp1b1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development.
Responsed Disease Injury of kidney [ICD-11: NB92.0]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Down regulation
Cell Process Cell proliferation
Cell apoptosis
In-vitro Model NRK-52E Normal Rattus norvegicus CVCL_0468
In-vivo Model Rats were anesthetized and incised through the midline of the abdomen, and the left renal vertebral arch and arteries were blocked for 45 min, thereby resulting in left kidney ischemia. At the same time, the right kidney was removed, further aggravating the degree of left kidney injury.
Transcription factor AP-2-alpha (TFAP2A)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation. When METTL3 was inhibited, m6A levels were accordingly decreased and cell apoptosis was suppressed in the H/R in vitro model. Based on MeRIP sequencing, Transcription factor AP-2-alpha (TFAP2A), cytochrome P-450 1B1 (cyp1b1), and forkhead box D1 (foxd1) were significantly differentially expressed, as was m6A, which is involved in the negative regulation of cell proliferation and kidney development.
Responsed Disease Injury of kidney [ICD-11: NB92.0]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell apoptosis
In-vitro Model NRK-52E Normal Rattus norvegicus CVCL_0468
In-vivo Model Rats were anesthetized and incised through the midline of the abdomen, and the left renal vertebral arch and arteries were blocked for 45 min, thereby resulting in left kidney ischemia. At the same time, the right kidney was removed, further aggravating the degree of left kidney injury.
Transcriptional coactivator YAP1 (YAP1)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [2]
Response Summary METTL14 promotes renal ischemic reperfusion injury via suppressing Transcriptional coactivator YAP1 (YAP1).
Responsed Disease Injury of kidney [ICD-11: NB92.0]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
Target Regulation Down regulation
Pathway Response Hippo signaling pathway hsa04390
Cell Process Cell proliferation and metastasis
In-vitro Model HK2 Normal Acipenser baerii CVCL_YE28
Metastasis associated lung adenocarcinoma transcript 1 (MALAT1)
In total 1 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [3]
Response Summary ALKBH5 could up-regulate Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) expression by demethylation. Furthermore, dexmedetomidine inhibited the expression of ALKBH5 in LPS-treated HK-2 cells. Dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which provides potential targets for the prevention and treatment of sepsis-induced kidney injury. Dexmedetomidine suppressed the biological behavior of HK-2 cells treated with LPS by inhibiting the expression of ALKBH5 in vitro, which provides potential targets for the prevention and treatment of sepsis-induced kidney injury.
Responsed Disease Injury of kidney [ICD-11: NB92.0Z]
Target Regulator RNA demethylase ALKBH5 (ALKBH5) ERASER
Target Regulation Up regulation
Cell Process Cell cycle
Cell proliferation
Cell apoptosis
In-vitro Model HK2 Normal Acipenser baerii CVCL_YE28
References
Ref 1 METTL3 contributes to renal ischemia-reperfusion injury by regulating Foxd1 methylation. Am J Physiol Renal Physiol. 2020 Nov 1;319(5):F839-F847. doi: 10.1152/ajprenal.00222.2020. Epub 2020 Sep 21.
Ref 2 The N6-methyladenosine mRNA methylase METTL14 promotes renal ischemic reperfusion injury via suppressing YAP1. J Cell Biochem. 2020 Jan;121(1):524-533. doi: 10.1002/jcb.29258. Epub 2019 Jul 18.
Ref 3 Dexmedetomidine Suppressed the Biological Behavior of HK-2 Cells Treated with LPS by Down-Regulating ALKBH5. Inflammation. 2020 Dec;43(6):2256-2263. doi: 10.1007/s10753-020-01293-y.