Role of macrophages in cardiorenal syndrome development in patients with myocardial infarction

Kercheva, M. A.; Рябов, В. В.

doi:10.15829/1560-4071-2021-4309

Cited by 4 publications

(3 citation statements)

References 50 publications

(91 reference statements)

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“…In the process of continuous damage, persistent infiltration of the kidney by M2 macrophages can lead to constant production of several growth factors that facilitate healing the wound, and what was initially triggered as a reparative mechanism can subsequently be unfavorable and cause irreversible fibrosis and progressive renal tissue destruction [25]. Evidence is available describing experimental models of chronic renal diseases, such as diabetic nephropathy in animals, in which macrophages cause a shift toward chronic activation of the M2 phenotype in later periods of the disease, which eventually leads to the development of glomerulosclerosis, interstitial tubular fibrosis and, ultimately, renal failure [37,38]. Perhaps this shift was the reason for the reduction in the amount of kidney CD206+ cells in our sample in patients with CKD.…”

Section: Discussionmentioning

confidence: 99%

Macrophages of the “Heart-Kidney” Axis: Their Dynamics and Correlations with Clinical Data and Outcomes in Patients with Myocardial Infarction

Kercheva

Ryabov

Gombozhapova

et al. 2022

JPM

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Changes in the macrophage infiltration of kidneys in rodents under ischemic conditions may affect cardiac macrophages and lead to development of adaptive cardiac remodeling. The aim of our study was to translate experimental findings into clinically relevant applications and assess the features of macrophage infiltration of the kidney and its correlations with changes in macrophage infiltration of the myocardium and with clinical data in patients who experienced a fatal myocardial infarction (MI). We examined fragments of both organs taken from patients (n = 30) who suffered from fatal MI. Macrophage infiltration was assessed by immunohistochemistry. Macrophage infiltration of the kidneys in patients with fatal MI is heterogeneous. The early period of MI was shown to be characterized by the prevalence of CD163+ and CD68+ cells, and in the long-term period by only CD163+ cells. However, only the level of CD206+ cells in the kidneys showed the dynamics representing the late MI period. Its decrease accompanied increase in the numbers of cardiac CD68+, CD163+, CD206+, and stabilin-1+ cells in the infarct area. Kidney CD206+ cells had more correlations with cardiac macrophages than other cells, and the presence of these cells also correlated with impairment of renal function and early death.

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Section: Discussionmentioning

confidence: 99%

Macrophages of the “Heart-Kidney” Axis: Their Dynamics and Correlations with Clinical Data and Outcomes in Patients with Myocardial Infarction

Kercheva

Ryabov

Gombozhapova

et al. 2022

JPM

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“…Currently acute myocardial ischemia and cardiomyocytes’ death that occur during MI are considered to trigger a two-phase inflammatory response in the damaged area of the myocardium [ 16 , 17 ]. Cells of the immune system (monocytes/macrophages) are key participants in this process [ 18 , 19 ]. Circulating monocytes migrate to the affected area (myocardium) with the blood flow and differentiate into M1 macrophages of the pro-inflammatory phenotype [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Characteristics of the Cardiosplenic Axis in Patients with Fatal Myocardial Infarction

Kercheva

Ryabov

Trusov

et al. 2022

Life

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Myocardial ischemia triggers neurohumoral activation of the cardiosplenic axis. In rodents, adverse outcomes occur upon prolonged entrance of mononuclear cells from the spleen into myocardial tissue. The purpose of this study is to assess the features of spleen structure in patients with fatal myocardial infarction (MI), the dynamics of macrophage infiltration of the spleen and its relationship with cardiac macrophage infiltration and unfavorable outcomes. Using immunohistochemistry techniques, we analyzed the macrophage infiltration of the spleen and myocardium sections collected from patients (n = 30) with fatal MI. The spleen of the patients was decreased and showed a predominance of red pulp with a high concentration of CD68+ and stabilin-1+ cells. The white pulp contained many medium and small follicles and a lower concentration of CD68+ and stabilin-1+ cells, which was comparable to that in the infarct area of the myocardium. The concentration of CD68+ and stabilin-1+ cells increased in the myocardium in the late period of MI, but did not show any dynamics in the spleen. A high number of CD68+ cells in the red pulp and reduced concentration of stabilin-1+ cells in the white pulp were associated with unfavorable post-infarction outcomes. These fundamental findings could be a basis for the development of new personalized therapeutic and diagnostic approaches for the treatment of MI and its complications.

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“…Changed polarization of macrophages (mf) in the kidneys induced by ischemia enhances the release of granulocyte-macrophage colony-stimulating factor into the bloodstream, which in turn causes subsequent polarization of myocardial mf into the regenerative M2 type and is associated with the development of fibrosis and adaptive myocardial hypertrophy [5]. However, clinical data on this interaction of innate immune cells along the heart-kidney axis are limited [7,8]. In our previous study, we investigated the composition of mf in the kidneys and its relationship with changes in mf infiltration into the heart, and with an adverse course of the disease in patients with fatal MI.…”

Section: Introductionmentioning

confidence: 99%

Macrophages of the Cardiorenal Axis and Myocardial Infarction

et al. 2023

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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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Role of macrophages in cardiorenal syndrome development in patients with myocardial infarction

Cited by 4 publications

References 50 publications

Macrophages of the “Heart-Kidney” Axis: Their Dynamics and Correlations with Clinical Data and Outcomes in Patients with Myocardial Infarction

Macrophages of the “Heart-Kidney” Axis: Their Dynamics and Correlations with Clinical Data and Outcomes in Patients with Myocardial Infarction

Characteristics of the Cardiosplenic Axis in Patients with Fatal Myocardial Infarction

Macrophages of the Cardiorenal Axis and Myocardial Infarction

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