Fig. 1.The mechanisms of TRPC5 in the cardiovascular and related
systems are outlined. First, under the stimulation of hypoxia, ox-LDL, or its
activator, TRPC5 can cause endothelial cells damage and dysfunction, smooth
muscle cell proliferation, atherosclerosis and high blood pressure by increasing
inflammatory response, ROS, senescence and apoptosis. TRPC5 can also cause renal
filtration barrier damage by injuring podocyte through the above mechanisms.
Furthermore, TRPC5 can enhance the transcription of cardiac hypertrophy gene by
regulating Ca/CaN/NFAT, leading to cardiac hypertrophy. Finally, TRPC5 can also
regulate BDNF and downstream signaling pathway to cause anxiety and depression
and other emotional disorders. AS = atherosclerosis; BDNF = brain derived
neurotrophic factor; EC = endothelial cell; ERK = extracellular regulated protein
kinases; HIF-1 = hypoxia inducible factor-1; HP = hypertension;
NFAT = nuclear factor of activated T cells; NF-B = nuclear transcription
factor-B; Ox-LDL = oxidized low-density lipoprotein; ROS = reactive
oxygen species; SMC = smooth muscle cell.