It increases interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-18 (IL-18) abundance and miR-133a expression, inhibits NF-κB, and decreases phosphorylation of the ASK1/MKK7/JNK pathway in cardiomyocytes, causing cardiac inflammation and fibrosis [143,144,145,146]. This evidence concerns the gene IL18 and inflammation.