A szívizom apoptosisának molekuláris szabályozása.

P. Andréka, Z. Nádházi, G. Müzes, N. H. Bishopric

Research output: Article

Abstract

Since apoptosis was described as a process distinct from necrosis, there have been many studies of programmed cell death in diseases, especially immunological diseases. Because cardiac myocytes are terminally differentiated cells, they have typically been assumed to die exclusively by necrosis. However, during the last six to seven years this view has been challenged by several studies demonstrating that a significant number of myocytes undergo apoptosis in myocardial infarction, heart failure, myocarditis, arrhythmogen right ventricular dysplasia, and immune rejection after cardiac transplantation, as well as in other conditions of stress. These are potentially very important observations, because apoptosis--unlike necrosis--can be blocked or reversed at early stages. The tracking of cytoprotective and apoptotic signal transduction pathways has proceeded rapidly with important new insights into the roles of mitochondria-dependent pathway, Bcl-2 protein family, p38 mitogen-activated protein kinase, extracellular signal-regulated kinase and c-Jun N-terminal kinase in cell fate. New studies have demonstrated that specific inhibition of apoptosis and activation of cytoprotective mechanisms, based on the better understanding of the intracellular signaling pathways, can significantly protect cardiac myocytes. This review will assess progress in cardiac myocyte apoptosis research and report on the current status of anti-apoptotic therapy in acute and chronic heart diseases.

Original languageHungarian
Pages (from-to)1717-1724
Number of pages8
JournalOrvosi Hetilap
Volume142
Issue number32
Publication statusPublished - aug. 12 2001

Fingerprint

Apoptosis
Cardiac Myocytes
Necrosis
JNK Mitogen-Activated Protein Kinases
Immune System Diseases
Extracellular Signal-Regulated MAP Kinases
Myocarditis
p38 Mitogen-Activated Protein Kinases
Heart Transplantation
Muscle Cells
Heart Diseases
Signal Transduction
Mitochondria
Chronic Disease
Cell Death
Heart Failure
Myocardial Infarction
Proteins
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Andréka, P., Nádházi, Z., Müzes, G., & Bishopric, N. H. (2001). A szívizom apoptosisának molekuláris szabályozása. Orvosi Hetilap, 142(32), 1717-1724.

A szívizom apoptosisának molekuláris szabályozása. / Andréka, P.; Nádházi, Z.; Müzes, G.; Bishopric, N. H.

In: Orvosi Hetilap, Vol. 142, No. 32, 12.08.2001, p. 1717-1724.

Research output: Article

Andréka, P, Nádházi, Z, Müzes, G & Bishopric, NH 2001, 'A szívizom apoptosisának molekuláris szabályozása.', Orvosi Hetilap, vol. 142, no. 32, pp. 1717-1724.
Andréka P, Nádházi Z, Müzes G, Bishopric NH. A szívizom apoptosisának molekuláris szabályozása. Orvosi Hetilap. 2001 aug. 12;142(32):1717-1724.
Andréka, P. ; Nádházi, Z. ; Müzes, G. ; Bishopric, N. H. / A szívizom apoptosisának molekuláris szabályozása. In: Orvosi Hetilap. 2001 ; Vol. 142, No. 32. pp. 1717-1724.
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