Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

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.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

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
Read the A–D evidence level guide

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.

How we grade evidence
HumansNeoplasmsMetabolic DiseasesAutoimmune DiseasesInflammationReactive Oxygen SpeciesRNA, MessengerAdenosineGene Expression ProfilingEpigenesis, Genetic

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