Interleukin-6 deficiency attenuates angiotensin II-induced cardiac pathogenesis with increased myocyte hypertrophy

Schematic diagram showing the development of cardiomyopathy under the regulation of IL-6 during AngII-stimulation. During AngII stimulation, IL-6 expression increases in cardiomyocytes and activates STAT3. STAT3 phosphorylation promotes its nucleus translocation. On one hand, phosphorylated STAT3 (p-STAT3) facilitates the transcription of genes associated with inflammation; on the other hand, p-STAT3 also strengthens the inhibitory effect of EndoG on MEF2A, resulting in alleviated myocyte hypertrophy. AngII also affects the EndoG-MEF2A signaling pathway by inhibiting EndoG expression, causing increased cardiac hypertrophy. Moreover, AngII promotes myocardium apoptosis via upregulating the ratio of Bax/Bcl-2.Dashed arrows: our hypothesis in the study.308