Skip to main content
. Author manuscript; available in PMC: 2024 Jun 14.
Published in final edited form as: Pediatr Res. 2019 Oct 24;87(2):309–318. doi: 10.1038/s41390-019-0581-7

Table 1.

Differential exercise regulation of monocyte genes previously associated with inflammation and/or CAD

Gene CAD Exercise Possible mechanisms
CD36 Facilitates scavenging of modified LDL and activates inflammatory pathways131
TLR4 Pathogenesis and destabilization of atherosclerotic plaques132
VCAN Versican is involved in advanced lesions of atherosclerosis at the borders of lipid-filled necrotic cores as well as at the plaque–thrombus interface133
DNAJB6 Controls HSP function, known to be a key immune modulator in atherosclerotic plaques134
FAM198B As yet unknown
HIST1H2BG Histone modification is a critical component of a transcriptional cascade regulating SMC proliferation and might play a role in the development of proliferative vascular diseases135

All data from human subjects. Data from coronary artery disease (CAD) patients is derived from previous studies. The exercise data is from our recent study in healthy people