29 m 6 A-RNA Methylation (Epitranscriptomic) Regulators Are Regulated in 41 Diseases including Atherosclerosis and Tumors Potentially via ROS Regulation - 102 Transcriptomic Dataset Analyses
Liu M., Xu K., Saaoud F., Shao Y., Zhang R., Lu Y.
Laboratory Study on Chronic Kidney Disease, Autoimmune Research, published in J Immunol Res (2022) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- J Immunol Res (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 35211628
- PMCID
- PMC8863469
- DOI
- 10.1155/2022/1433323
- Citations
- 32
Abstract (original English)
We performed a database mining on 102 transcriptomic datasets for the expressions of 29 m 6 A-RNA methylation (epitranscriptomic) regulators (m 6 A-RMRs) in 41 diseases and cancers and made significant findings: (1) a few m 6 A-RMRs were upregulated; and most m 6 A-RMRs were downregulated in sepsis, acute respiratory distress syndrome, shock, and trauma; (2) half of 29 m 6 A-RMRs were downregulated in atherosclerosis; (3) inflammatory bowel disease and rheumatoid arthritis modulated m 6 A-RMRs more than lupus and psoriasis; (4) some organ failures shared eight upregulated m 6 A-RMRs; end-stage renal failure (ESRF) downregulated 85% of m 6 A-RMRs; (5) Middle-East respiratory syndrome coronavirus infections modulated m 6 A-RMRs the most among viral infections; (6) proinflammatory oxPAPC modulated m 6 A-RMRs more than DAMP stimulation including LPS and oxLDL; (7) upregulated m 6 A-RMRs were more than downregulated m 6 A-RMRs in cancer types; five types of cancers upregulated ≥10 m 6 A-RMRs; (8) proinflammatory M1 macrophages upregulated seven m 6 A-RMRs; (9) 86% of m 6 A-RMRs were differentially expressed in the six clusters of CD4 + Foxp3 + immunosuppressive Treg, and 8 out of 12 Treg signatures regulated m 6 A-RMRs; (10) immune checkpoint receptors TIM3, TIGIT, PD-L2, and CTLA4 modulated m 6 A-RMRs, and inhibition of CD40 upregulated m 6 A-RMRs; (11) cytokines and interferons mo
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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