ArticleVirchows Archiv : an international journal of pathology1997
Membrane attack complex of complement and 20 kDa homologous restriction factor (CD59) in myocardial infarction.
Article in Virchows Archiv : an international journal of pathology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 citing papers in PubMed, 13 citations in OpenAlex.
- Membrane Attack Complex in Myocardial Ischemia/Reperfusion Injury: A Systematic Review for Post Mortem Applications.Diagnostics (Basel, Switzerland) · 2020Review
- Molecular tissue changes in early myocardial ischemia: from pathophysiology to the identification of new diagnostic markers.International journal of legal medicine · 2018Review
- Possible role of complement factors and their inhibitors in the myocardial infarction: an immunohistochemical study.Central-European journal of immunology · 2014Article
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7 authors at 2 institutions in 1 country.
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Abstract
In order to investigate the mechanism of deposition of the complement membrane attack complex (MAC) in cardiomyocytes in areas of human myocardial infarction, the 20 kDA homologous restriction factor of complement (HRF20; CD59) and complement components (Clq. C3d and MAC) were analysed immunohistochemically using specific antibodies. Myocardial tissues obtained at autopsy from nine patients who died of acute myocardial infarction were fixed in acetone and embedded in paraffin. The ages of the infarcts ranged from about 3.5 h to 12 days. In cases of myocardial infarction of 20 h or less, MAC deposition was shown in the infarcted cardiomyocytes without loss of HRF20. Where the duration was 4 days or more, the cardiomyocytes with MAC deposition in the infarcted areas also showed complete loss of HRF20. Outside the infarcts, HRF20 in the cardiomyocytes was well preserved without MAC deposition. The present study suggests that the initial MAC deposition in dead cardiomyocytes can occur as a result of degradation of plasma-membrane by a mechanism independent of complement-mediated injury to the membrane. Loss of HRF20 from dead cardiomyocytes may not be the initial cause of MAC deposition, but may accelerate the deposition process of MAC in later stages of infarction.
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