Expression of bcl-2 and Bax protein in the failing human heart —an inhibitor or accelerator of apoptosis?

Abstract

Abstract: In general, myocyte death in myocardial infarctions (MI) is attributed to necrosis, but recently the involvement of apoptosis has been suggested. Loss of myocytes is an important mechanism in the development of cardiac failure of either ischemic or nonischemic origin. The expression of two proto-oncogenes influence apoptosis. Myocytes with positive bcl-2 immunoreactivity were seen in the heart of acute MI, localized only in the salvaged areas surrounding the infarcted tissues. Myocytes with overexpressed positive Bax immunoreactivity were observed in the salvaged areas of old MI.

Key words: MI, apoptosis, bcl-2, Bax

CHEN YIJIU;ET AL.(INSTITUTE OF FORENSIC SCIENCES;MINISTRY OF JUSTICE;SHANGHAI 000;P.R.CHINA). Expression of bcl-2 and Bax protein in the failing human heart —an inhibitor or accelerator of apoptosis?[J]. , 2000, 0(1): 10-11+6.

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Expression of bcl-2 and Bax protein in the failing human heart —an inhibitor or accelerator of apoptosis?

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