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Eur J Cardiothorac Surg 2009;35:553-554. doi:10.1016/j.ejcts.2008.11.021
Copyright © 2009, European Association for Cardio-thoracic Surgery. Published by Elsevier. All rights reserved.
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Letters to the Editor

Can cardiac fibrosis be prevented? Mast cell inhibition versus anti-chymase activity

Ahmet Akgul*

Department of Cardiovascular Surgery, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey

Received 19 October 2008; accepted 19 November 2008.

* Corresponding author. Tel.: +90 312 306 1444. (Email: aakgul{at}turkiyeklinikleri.com).

Key Words: Mast cell • Chymase • Fibrosis • TGF-β1 • Basic FGF

I have read with great interest the work by Kanemitsu et al. [1]. They demonstrated that chronic inhibition of chymase prevented fibrosis and maintained left ventricle function after left ventricular repair in a rat chronic myocardial infarction model.

Heart failure is a chronic syndrome in which cardiac remodeling plays an important role in the pathogenesis; furthermore, cardiac mast cells may be one of the main-stays of pathologic mechanism according to the current studies [2,3]. Protein kinase C signaling is a relatively new signal transduction pathway of mast cell degradation which currently attracts attention. Palaniyandi and co-workers introduced protein kinase C inhibition to prevent cardiac mast cell degranulation without affecting mast cell density and they performed eacgrV1-2 treatment for rat cardiac mast cell degranulation and decreased myocardial fibrosis [4].

Although Kanemitsu and co-workers underlined that inhibition of fibrosis established by cardiac chymase via transforming growth factor-β, our study also demonstrated that chymase, mediator of mast cell degranulation, related with myocardial fibrosis especially by basic-FGF [2].

These new findings and our previous studies [2–5] demonstrate that chymase-positive mast cells were associated with not only increased fibrosis but degradation of these cells may contribute in decreased cardiac inflammation and remodeling.

One of my concerns about this excellent study by Kanemitsu is that he and his colleagues may be performing chronic chymase inhibition with oral medications, when according to previous studies, cardiac mast cells have several mediators as tryptase, 5-lipoxygenase, cytokins, histamin, serglycin, proteoglycans, carboxypeptidase. Chymase, tryptase and carboxypeptidase are also known as mast cell-specific proteases. Recent studies show promising progress of mast cell specific proteases, so how can Kenemitsu help us by reducing fibrosis by only preventing one mast – cell specific protease, instead of direct mast cells inhibition?

References

  1. Kanemitsu H, Takai S, Tsuneyoshi H, Yoshikawa E, Nishina T, Miyazaki M, Ikeda T, Komeda M. Chronic chymase inhibition preserves cardiac function after left ventricular repair in rats. Eur J Cardiothorac Surg 2008;33(1):25-31.[Abstract/Free Full Text]
  2. Akgul A, Skrabal CA, Thompson LO, Loebe M, Lafuente JA, Noon GP, Youker KA. Role of mast cells and their mediators in failing myocardium under mechanical support. J Heart Lung Transplant 2004;23(6):709-715.[CrossRef][Medline]
  3. Akgul A, Youker KA, Noon GP, Loebe M. Quantitative changes in mast cell populations after left ventricular assist device implantation. ASAIO J 2005;51(3):275-280.[CrossRef][Medline]
  4. Palaniyandi SS, Inagaki K, Mochly-Rosen D. Mast cells and {varepsilon}PKC: a role in cardiac remodeling in hypertension-induced heart failure. J Mol Cell Cardiol 2008;45(6):779-786.[CrossRef][Medline]
  5. Akgul A. Cardiac mast cells [In Turkish]. Turkiye Klinikleri J Cardiovasc Sci 2007;21:63-65.



This article has been cited by other articles:


Home page
 Eur. J. Cardiothorac. Surg.Home page
H. Kanemitsu, S. Takai, M. Miyazaki, and M. Komeda
Reply to Agkul
Eur. J. Cardiothorac. Surg., March 1, 2009; 35(3): 554 - 555.
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