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Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

RNA m6A Modification in Immunometabolism: Context-Dependent Mechanisms and Therapeutic Perspectives

  • Qiong Fang1
  • Wei Li1
  • Yongqing Cai1
  • Shuyi Zhang2
  • Xinzhi Tang1
  • Chu Chu1
  • Miaomiao Zhou1
  • Fang Li1
  • Zhen Zhang1
  • Xia Li1,2
  1. 1Innovative Institute of Chinese Medicine and Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, China
  2. 2College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250355, China
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Abstract

N6-methyladenosine (m6A) regulates RNA fate and has been linked to immune cell function and metabolic adaptation. This narrative review examines selected studies across innate, adaptive, and tissue-resident immune populations, focusing on the cellular origin, target transcript, and experimental evidence supporting each mechanism. Metabolic inputs, including α-ketoglutarate, lactate, and D-2-hydroxyglutarate, can influence m6A regulatory pathways, while m6A-dependent RNA regulation can alter metabolic enzymes, transporters, and immune responses. We discuss these findings within a proposed metabolite–m6A–immune framework; reciprocal relationships demonstrated in separate settings do not establish a closed feedback circuit in every cell population or disease model. We distinguish direct metabolic measurements from changes in signaling, survival, differentiation, and inferred pathway activity, and consider how tissue context and target selection may account for contrasting effects of the same regulator. Representative pharmacological studies of METTL3, FTO, and YTH domain readers are considered alongside interventions with less well-defined target specificity and early clinical development of METTL3 inhibition. The available evidence supports context-dependent mechanisms and therapeutic hypotheses, while clinical benefit, cellular selectivity, and long-term safety remain unresolved for the applications discussed.

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Cite

BibTeXRIS
BibTeX
@article{fang2026modification,
  title = {{RNA m6A Modification in Immunometabolism: Context-Dependent Mechanisms and Therapeutic Perspectives}},
  author = {Qiong Fang and Wei Li and Yongqing Cai and Shuyi Zhang and Xinzhi Tang and Chu Chu and Miaomiao Zhou and Fang Li and Zhen Zhang and Xia Li},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27219566},
  url = {https://www.mdpi.com/1422-0067/27/21/9566},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - RNA m6A Modification in Immunometabolism: Context-Dependent Mechanisms and Therapeutic Perspectives
AU  - Qiong Fang
AU  - Wei Li
AU  - Yongqing Cai
AU  - Shuyi Zhang
AU  - Xinzhi Tang
AU  - Chu Chu
AU  - Miaomiao Zhou
AU  - Fang Li
AU  - Zhen Zhang
AU  - Xia Li
PY  - 2026
DA  - 2026/10/26
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27219566
UR  - https://www.mdpi.com/1422-0067/27/21/9566
AB  - N6-methyladenosine (m6A) regulates RNA fate and has been linked to immune cell function and metabolic adaptation. This narrative review examines selected studies across innate, adaptive, and tissue-resident immune populations, focusing on the cellular origin, target transcript, and experimental evidence supporting each mechanism. Metabolic inputs, including α-ketoglutarate, lactate, and D-2-hydroxyglutarate, can influence m6A regulatory pathways, while m6A-dependent RNA regulation can alter metabolic enzymes, transporters, and immune responses. We discuss these findings within a proposed metabolite–m6A–immune framework; reciprocal relationships demonstrated in separate settings do not establish a closed feedback circuit in every cell population or disease model. We distinguish direct metabolic measurements from changes in signaling, survival, differentiation, and inferred pathway activity, and consider how tissue context and target selection may account for contrasting effects of the same regulator. Representative pharmacological studies of METTL3, FTO, and YTH domain readers are considered alongside interventions with less well-defined target specificity and early clinical development of METTL3 inhibition. The available evidence supports context-dependent mechanisms and therapeutic hypotheses, while clinical benefit, cellular selectivity, and long-term safety remain unresolved for the applications discussed.
SN  - 1422-0067
ER  -