Fibronectin has two different forms, cellular and plasma fibronectin. Cellular fibronectin is expressed by fibroblasts and is deposited locally into the ECM. In general, locally-produced cellular fibronectin appears at the injury site within the early phase after tissue injury. Plasma fibronectin is synthesized by hepatocytes and secreted into the blood plasma. Plasma fibronectin levels have been shown to increase after major trauma resulting in vascular tissue damage and inflammation such as atherosclerosis and ischemic diseases. Previous studies suggested that mechanical stress contributes to injury and fibrosis by inducing epithelial-mesenchymal transition via a mechanism driven by TGF-b1 and WNT signaling. We also investigated the relation between high glucose and WNT10A in COS1 cells. High glucose induces caspase-3- dependent apoptosis in fibroblasts, and activation of caspase caused by high glucose stress is independent of Fas/FasL signaling pathways system. Activation of caspase-3 requires proteolytic cleavage of its inactive zymogen into active subunits. Cleaved caspase-3 causes apoptosis by degrading PARP. Our results show that WNT10A overexpression COS1 cells weaker expressed cleaved caspase-3 and PARP than control cells. WNT10A protected cells from apoptosis caused by high glucose stress. Consequently, a proliferation of WNT10A-overexpressing COS1 cells was small reduction than control cells. 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors are used as therapy for hyperlipidemia. Statins inhibit kidney fibrosis and inflammation in rats, and inhibits fibronectin expression in human airway fibroblasts. Several studies have reported that statins are anti-inflammatory and block proliferation by G1 arrest of the cell cycle. Our investigation also indicated that simvastatin suppressed proliferation of COS1 via inducing apoptosis regardless of WNT10A expression. Our work suggests that it will be important to study the effects of statins during kidney fibrosis in a clinical setting. Myocardial infarction induces Galiellalactone cardiac sympathetic nerve sprouting in humans and in animal models. Cardiac nerve growth factor is a major neurotrophin correlated with sympathetic nerve sprouting, and NGF plays an important role in synapse formation and axonal growth during sympathetic neuron development. Zhou et al. demonstrated that MI increased cardiac NGF and growth associated protein 43 expression in the infarcted area. NGF and GAP43 were then transported DL-AP4 Sodium salt retrogradely to the left stellate ganglion, which resulted in sympathetic nerve sprouting in the noninfarcted area. However, excessive nerve sprouting suppressed the functions of transient outward current and inward rectifier current, thereby increasing the susceptibility to ventricular arrhythmias. Accordingly, inhibition of sympathetic nerve sprouting processes may provide an effective therapy to prevent arrhythmias.