[Retracted] Tongyang Huoxue Decoction (TYHX) Ameliorating Hypoxia/Reoxygenation-Induced Disequilibrium of Calcium Homeostasis and Redox Imbalance via Regulating Mitochondrial Quality Control in Sinoatrial Node Cells

Figure 7

The mechanism of TYHX-regulating cardiac pacing function through mitochondrial quality control and calcium homeostasis. Figure legend: mitochondrial quality control can regulate the energy metabolism of cells (including endothelial cells, cardiomyocytes, and sinoatrial node cells), mitochondrial oxidative stress signaling pathways, ROS production, redox balance, cell death/apoptosis, calcium homeostasis, and inflammation. An important biological process of the cell growth cycle. H/R can cause phosphorylated Drp1 to accumulate around the outer mitochondrial membrane and induce Fis1-regulated mitochondrial fission. The transient decrease of mitochondrial membrane potential level is accompanied by phosphorylation or dephosphorylation of FUNDC1. The interaction of Parkin and LC3 induces the occurrence of mitophagy. This process is often accompanied by the occurrence of mitochondrial biosynthesis. H/R-induced mitochondrial quality control disorder will further break the balance of mitochondrial calcium release/calcium contraction (regulated by SERCA2a and RyR2), which led to the imbalance of mitochondrial homeostasis and calcium homeostasis. The process of sinoatrial node cell death/apoptosis will be accelerated. A variety of active ingredients in TYHX that can regulate Parkin/ATG-led mitophagy and remove excess mitochondrial fragment. Inhibit the expression of Fis1, increase the expression of Mfn on the mitochondrial membrane, and promote the occurrence of mitochondrial fusion. And by adjusting PGC1α and Tfam to improve the mitochondrial biosynthesis effect, adjust the mitochondrial quality control and the calcium homeostasis mechanism dominated by SERCA2a and RyR2.