[Frontiers in Bioscience 17, 221-231, January 1, 2012]

Angiotensin II induces inflammation leading to cardiac remodeling

Lixin Jia1,2, Yulin Li1, Chuanshi Xiao2, Jie Du1

1The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing 100029, China, 2Department of Cardiology, the Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China


1. Abstract
2. Introduction
3. Ang II and inflammation
4. Ang II and chemokines
5. Ang II and inflammatory cells
6. Ang II and imbalance of inflammatory or anti-inflammatory cytokines
7. Ang II and pro-inflammatory signaling pathway
8. Ang II and myofibroblasts
9. Perspectives
10. Acknowledgement
11. References


Hypertension, especially for elevated renin-angiotensin II (Ang II), induces cardiac fibrosis and remodeling. Ang II, acting via its receptors, causes both hemodynamic and nonhemodynamic effects. These effects trigger a series of inflammatory responses. Recent studies have demonstrated that hypertension stimulates infiltration of leukocytes into heart, and interaction among macrophages, T cells, and monocytic fibroblast precursor cells regulates the imbalance of pro-inflammatory and anti-inflammatory factors. Several studies have demonstrated that the inflammatory microenvironment in hypertensive heart promotes a forward feedback infiltration of leukocytes, differentiation of monocytes, and formation of myofibroblasts. An increased number of myofibroblasts, the dominant source of extracellular matrix production, results in deposition of collagen and cardiac remodeling. A thorough understanding of the pathological process underlying hypertension-induced cardiac remodeling may help in prevention and treatment.