ABSTRACT
The negative effects of low temperature can readily induce a variety of diseases. We sought to understand the reasons why cold stress induces disease by studying the mechanisms of fine-tuning in macrophages following cold exposure. We found that cold stress triggers increased macrophage activation accompanied by metabolic reprogramming of aerobic glycolysis. The discovery, by genome-wide RNA sequencing, of defective mitochondria in mice macrophages following cold exposure indicated that mitochondrial defects may contribute to this process. In addition, changes in metabolism drive the differentiation of macrophages by affecting histone modifications. Finally, we showed that histone acetylation and lactylation are modulators of macrophage differentiation following cold exposure. Collectively, metabolism-related epigenetic modifications are essential for the differentiation of macrophages in cold-stressed mice, and the regulation of metabolism may be crucial for alleviating the harm induced by cold stress.
Subject(s)
Animals , Mice , Acetylation , Cold-Shock Response , Epigenesis, Genetic , Macrophages/metabolism , Mitochondria/metabolismABSTRACT
Stereotactic body radiotherapy (SBRT/SABR) has become an important option in the treatment of early non-small-cell lung cancer (NSCLC). Radiation pneumonitis (RP) is the main side effect of early NSCLC patients after SBRT/SABR. Patient factors, tumor factors and treatment factors are all associated with the occurrence of RP in early NSCLC patients after SBRT/SABR. In recent years, relevant studies have further clarified the relationship between these factors and RP. In addition, the prediction factors related to RP occurrence are further discussed. In this paper, relevant research progresses in recent years were reviewed.