“…The CD36 gene transcription is regulated by peroxisome proliferator-activated receptor-g (PPARg) (Nagy et al, 1998;Tontonoz et al, 1998), nuclear erythroid-related factor 2 (Nrf2) (Ishii et al, 2004;Olagnier et al, 2011), as well as by signal transducer and activator of transcription 1 (STAT1) (Kotla et al, 2017) pathways. In addition, CD36 expression can also be regulated by retinol-binding protein 4 (Liu et al, 2017b), protein kinase Cu (PKCu)/activating transcription factor 2 (Raghavan et al, 2018), epidermal growth factor receptor (Zeboudj et al, 2018), trimethylamine N-oxide (Geng et al, 2018), NACHT, LRR, and PYD domains-containing protein 3 inflammasome (Chen et al, 2018b), transient receptor potential vanilloid 4 (TRPV4) (Goswami et al, 2017), cellular communication network factor 3 (Shi et al, 2017), melanocortin 1 receptor (Rinne et al, 2017), cluster of differentiation 146 (CD146) (Luo et al, 2017), triggering receptor expressed on myeloid cells (Joffre et al, 2016), cyclophilin A (Ramachandran et al, 2016), and many others. Furthermore, CD36-mediated foam cell formation and atherosclerosis were negatively regulated by C1q/tumor necrosis factor-related protein 13 via autophagy/lysosomedependent degradation of CD36 (Wang et al, 2019a).…”