Inhibition of PGK1 attenuates autoimmune myocarditis by reprogramming CD4+ T cells metabolism.
Yang LuNing ZhaoYuwei WuShuaitao YangQiongfeng WuQian DongYimei DuPublished in: Cardiovascular research (2023)
Myocarditis usually causes inflammatory damage and fibrosis of the myocardium, resulting in dilated cardiomyopathy. Activated CD4+ T cells, such as Th1, Treg, especially Th17 cells, have been shown to mediate the pathogenesis of myocarditis. We found that glycolysis and PGK1 were significantly elevated in CD4+ T and Th17 cells in hearts with myocarditis. Inhibition of PGK1 leads to decreased glycolysis and increased ROS production and regulates Th17, Th1 and Treg differentiation, which may reduce inflammatory damage and delay the progression of dilated cardiomyopathy in myocarditis patients.
Keyphrases
- induced apoptosis
- oxidative stress
- cell cycle arrest
- end stage renal disease
- ejection fraction
- cell death
- newly diagnosed
- multiple sclerosis
- endoplasmic reticulum stress
- chronic kidney disease
- dna damage
- prognostic factors
- peritoneal dialysis
- cell proliferation
- patient reported outcomes
- reactive oxygen species
- pi k akt