IMR Press / FBL / Volume 17 / Issue 1 / DOI: 10.2741/3923

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Angiotensin II induces inflammation leading to cardiac remodeling
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1 The 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
2 Department of Cardiology, the Second Hospital of Shanxi Medical University, Taiyuan, 030001, Shanxi, China
Front. Biosci. (Landmark Ed) 2012, 17(1), 221–231;
Published: 1 January 2012
(This article belongs to the Special Issue CREG promotes vasculogenesis by activation of VEGFPI3KAkt pathway)

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.

Angiotensin II
Cardiac Remodeling
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