It has been shown that recurrent exposure to subclinical lipopolysaccharide (LPS) increases mortality and induces cardiac fibrosis in mice, which is not mediated by the common renin-angiotensin system.
Angiotensin II (Ang II), an effective component of renin-angiotensin system, plays a pivotal role in cardiac fibrosis, which may further contribute to heart failure.
This article further confirms the involvement of the renin-angiotensin system in cardiac fibrosis and illustrates the supportive roles of mineralocorticoids, endothelin, and novel signaling pathways.