NR1H4 and coronary atherosclerosis: The tissue-specific expression of FXR alters the mechanistic roles they play in maintaining BA homeostasis.[33] Modest concentrations of CDCA can interact with FXR to attenuate inflammation in vascular smooth muscle and prevent coronary atherosclerosis.[34] BAs can also prevent cardiac remodeling and hypertrophy by inhibiting nuclear factor-κB (NFκ-B), a transcription factor for several inflammatory mediators.[35]