Firstly, pCS and IS could induce significant cellular inflammation reaction, which is an important pathological mechanism for kidney injury [33, 34]; secondly, they promote kidney fibrosis and accelerate kidney disease and renal dysfunction [35–37]; thirdly, they promote cardiomyocyte apoptosis via NAPKH oxidase [38] and cardiac hypertrophy via AM p-activated protein kinase/uncoupling protein 2, respectively [39, 40]. This evidence concerns the gene UCP2 and cardiac hypertrophy.