Various atherogenic risk factors including physical insult (shear stress and heat), chemical stress (smoking, oxygen radicals, drugs, high sodium, and high glucose), infection (e.g., Chlamydia pneumoniae), and inflammation (LPS, inflammatory cytokines, and oxLDLs) possess the ability to regulate the expression or localization of HSP60 in ECs (Amberger et al., 1997; Hochleitner et al., 2000; Hirono et al., 2003; Wick et al., 2008, 2014; Kreutmayer et al., 2011, 2013; Mohammad and Kowluru, 2011; Zhao et al., 2015; Jakic et al., 2017). Here, HSPD1 is linked to infection.