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Macrophages of the Cardiorenal Axis and Myocardial Infarction

ORCID
0000-0003-1444-1037
Affiliation
Cardiology Division, Siberian State Medical University, 2 Moscovsky Trakt, 634055 Tomsk, Russia
Kercheva, Maria;
ORCID
0000-0002-4358-7329
Affiliation
Cardiology Division, Siberian State Medical University, 2 Moscovsky Trakt, 634055 Tomsk, Russia
Ryabov, Vyacheslav;
ORCID
0000-0003-1281-3714
Affiliation
Cardiology Division, Siberian State Medical University, 2 Moscovsky Trakt, 634055 Tomsk, Russia
Gombozhapova, Aleksandra;
ORCID
0000-0002-8543-6027
Affiliation
Cardiology Research Institute, Tomsk National Research Medical Center of the RAS, 111a Kievskaya Street, 634012 Tomsk, Russia
Stepanov, Ivan;
Affiliation
Laboratory of Translational and Cellular Biomedicine, National Research Tomsk State University, 36 Lenin Avenue, 634050 Tomsk, Russia
Kzhyshkowska, Julia

The aim of our study was to compare the features of macrophage (mf) composition of the kidneys in patients with fatal myocardial infarction (MI) and in patients without cardiovascular diseases (CVD). We used kidney fragments taken during autopsy. Macrophage infiltration was assessed by immunohistochemistry: antibodies CD68 were used as a common mf marker, CD80—M1 type mf marker, CD163, CD206, and stabilin-1—M2 type. Macrophage composition of the kidneys in patients with fatal MI was characterized by the predominance of CD163+ cells among studied cells, and the control group was characterized by the predominance of CD163+, CD206+, and CD68+. In patients with MI, biphasic response from kidney cells was characterized for CD80+ and CD206+: their number decreased by the long-term period of MI; other cells did not show any dynamics. The exact number of CD80+ cells in kidneys of individuals without CVD was slightly higher than in patients with MI, and the number of CD206+—strikingly predominant. Subsequent analysis of CD80+ and CD206+ cells in a larger sample, as well as comparison of data with results obtained from survivors of MI, may bring us closer to understanding whether the influence on these cells can serve as a new target in personalized therapy in postinfarction complications.

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