Cardiac remodeling

Activation of matrix metalloproteinases (MMP) is also involved in vascular and cardiac remodelling. For example, the fibrillar collagen matrix of the heart... 

Cardiac remodeling Genome expression resulting in molecular, cellular, and interstitial changes and manifested clinically as changes in size, shape, and function of the heart resulting from cardiac load or injury. 

These drugs have also been studied for possible use in other conditions. Clinical studies show distinct benefit in some patients with pulmonary arterial hypertension, and possible benefit in systemic hypertension, cystic fibrosis, and benign prostatic hyperplasia. Preclinical studies suggest that sildenafil may be useful in preventing apoptosis and cardiac remodeling after ischemia and reperfusion. 

FedakPW, Verma S, Weisel RD, Li RK. Cardiac remodeling and failure from molecules to man (parti). Cardiovasc Pathol. 2005 14 1-11. 

Sharpe N. Pharmacologic effects on cardiac remodeling. Curr Heart Fail Rep. 2004 1 9-13. 

Harada M, Qin Y Takano H, et al. G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes. Nat Med 2005 I 1(3)305-3 I I. 

Sun, Y., and Weber, K.T. 1998. Cardiac remodeling by fibrous tissue role of local factors and circulating hormones. Ann. Med. 30(Suppl. 1) 3—8. 

Bujak, M., and Frangogiannis, N.G., 2007. The role of TGF-beta signaling in myocardial infarction and cardiac remodeling. Cardiovasc. Res. 74 184-195. 

Fig. 12.1 Concentric and eccentric cardiac remodeling. In response to a systolic load, newly formed sarcomeres will be assembled in a parallel fashion leading to an increase in myocyte cell width. This mode of sarcomere assembly will result in a concentric pattern of cardiac hypertrophy characterized by an increase in wall thickness and reduction in chamber volume. In contrast, in response to a diastolic load, newly formed sarcomeres will be assembled in an in series pattern leading to an increase in myocyte cell length. This mode of sarcomere assembly will promote an eccentric pattern of cardiac hypertrophy characterized primarily by an increase in chamber volume. However, a modest increase in wall thickness will also occur because of the secondary increase in systolic wall stress associated with eccentric remodeling.

Palmen M, Daemen MJ, Bronsaer R, Dassen WR, Zandbergen HR, Kockx M, et al. Cardiac remodeling after myocardial infarction is impaired in IGF-1 deficient mice. Cardiovasc Res 2001 50 516-524. 

Hayakawa K, Takemura G, Kanoh M, Li Y, Koda M, Kawase Y, et al. Inhibition of granulation tissue cell apoptosis during the subacute stage of myocardial infarction improves cardiac remodeling and dysfunction at the chronic stage. Circulation 2003 108 104-109. 

Myocardial infarction Cardiac myocyte death Cardiac remodeling Cardiac myocyte death... 

Liao P, Georgakopoulos D, Kovacs A, et al. The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy. Proc Natl Acad Sci USA 2001 98 12,283-12,288. 

Barry DM, Xu H, Schuessler RB, Nerbonne JM. Functional knockout of the transient outward current, long-QT syndrome, and cardiac remodeling in mice expressing a dominant-negative Kv4 alpha subunit. Circ Res 1998 83 560—... 

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