Journal
CURRENT HYPERTENSION REPORTS
Volume 15, Issue 4, Pages 395-400Publisher
SPRINGER
DOI: 10.1007/s11906-013-0354-3
Keywords
Cardiac remodeling; Fibrosis; Arterial hypertension; Aldosterone; Angiotensin II; AngII; Renin-angiotensin-aldosterone system; RAAS; BNP; Galectin-3; Myocardium; Mineralocorticoid receptor; MR
Categories
Funding
- Inserm
- Universite Paris-Diderot
- Fondation de France
- Societe Francaise d'Hypertension Arterielle (SFHTA)
Ask authors/readers for more resources
Cardiac remodeling is a deleterious consequence of arterial hypertension. This remodeling results from cardiac transcriptomic changes induced by mechanical and hormonal factors. Angiotensin II and aldosterone often collaborate in pathological situations to induce hypertrophy of cardiomyocytes, vascular inflammation, perivascular and interstitial fibrosis, and microvascular rarefaction. Experimental models of transgenic mice overexpressing renin in liver, leading to increased plasma angiotensin II and severe hypertension, and mice overexpressing aldosterone-synthase in cardiomyocytes, leading to a doubling of intracardiac aldosterone concentration have shown that cardiac fibrosis in the heart depends on a balance between pro-fibrotic (TGF-, galectin-3) and anti-fibrotic (BNP, ANP) factors. Recent studies using cell-specific deletion of the mineralocorticoid receptor indicate that its activation in macrophages is a key step in the development of cardiac fibrosis in the setting of hemodynamic or hormonal challenges. This review focuses on the impact of inappropriate stimulation of aldosterone in the development of cardiac fibrosis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available