α‐Ketoglutarate plays an inflammatory inhibitory role by regulating scavenger receptor class a expression through N6‐methyladenine methylation during sepsis

Author:

Liang Gang12,Hu Jia‐Yan1,Liu Rou‐Jun1,Chao Yu‐Peng1,Hu Yi‐Fan1,Zheng Hong1,Pan Xin‐Yu1,Li Yuan‐Jing1,Gong Yang‐Hui1,Lin Chi1,Lin Jia‐Hao1,Wang Jia‐Dong1,Li Tong‐Xin1,Pan Jian‐Ping13,Guo Dong‐Yang13ORCID

Affiliation:

1. Department of Clinical Medicine Hangzhou City University School of Medicine Hangzhou P.R. China

2. Zhejiang University school of medicine Hangzhou P. R. China

3. Institute of Translational Medicine Hangzhou City University Hangzhou P.R. China

Abstract

AbstractSepsis arises from an uncontrolled inflammatory response triggered by infection or stress, accompanied by alteration in cellular energy metabolism, and a strong correlation exists between these factors. Alpha‐ketoglutarate (α‐KG), an intermediate product of the TCA cycle, has the potential to modulate the inflammatory response and is considered a crucial link between energy metabolism and inflammation. The scavenger receptor (SR‐A5), a significant pattern recognition receptor, assumes a vital function in anti‐inflammatory reactions. In the current investigation, we have successfully illustrated the ability of α‐KG to mitigate inflammatory factors in the serum of septic mice and ameliorate tissue damage. Additionally, α‐KG has been shown to modulate metabolic reprogramming and macrophage polarization. Moreover, our findings indicate that the regulatory influence of α‐KG on sepsis is mediated through SR‐A5. We also elucidated the mechanism by which α‐KG regulates SR‐A5 expression and found that α‐KG reduced the N6‐methyladenosine level of macrophages by up‐regulating the m6A demethylase ALKBH5. α‐KG plays a crucial role in inhibiting inflammation by regulating SR‐A5 expression through m6A demethylation during sepsis. The outcomes of this research provide valuable insights into the relationship between energy metabolism and inflammation regulation, as well as the underlying molecular regulatory mechanism.

Funder

National Natural Science Foundation of China

Natural Science Foundation of Zhejiang Province

Publisher

Wiley

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