Уважаемые коллеги, доброго времени суток! Мы начинаем обзор изданий в области Эндокринологии, диабета и метаболизма. Сегодня хотим представить вашему вниманию немецкое научное издание Diabetologia. Журнал имеет первый квартиль, издаётся в Springer Verlag, его SJR за 2021 г. равен 3,528, печатный ISSN - 0012-186X, электронный - 1432-0428, предметные области - Эндокринология, диабет и метаболизм, Медицина внутренних болезней. Вот так выглядит обложка:
Редактором является Хиндрик Мулдер, контактные данные - hindrik.mulder@med.lu.se, diabetologia-j@bristol.ac.uk.
К публикации принимаются оригинальные клинические, трансляционные и экспериментальные исследования по всем аспектам исследований диабета и смежных дисциплин, при условии, что они имеют научную ценность и представляют собой важный прогресс в знаниях.
Адрес издания - https://diabetologia-journal.org/
Пример статьи, название - CCR2-positive monocytes contribute to the pathogenesis of early diabetic retinopathy in mice. Заголовок (Abstract)
Aims/hypothesis
Accumulating evidence suggests that leucocytes play a critical role in diabetes-induced vascular lesions and other abnormalities that characterise the early stages of diabetic retinopathy. However, the role of monocytes has yet to be fully investigated; therefore, we used Ccr2−/− mice to study the role of CCR2+ inflammatory monocytes in the pathogenesis of diabetes-induced degeneration of retinal capillaries.
Methods
Experimental diabetes was induced in wild-type and Ccr2−/− mice using streptozotocin. After 2 months, superoxide levels, expression of inflammatory genes, leucostasis, leucocyte- and monocyte-mediated cytotoxicity against retinal endothelial cell death, retinal thickness and visual function were evaluated. Retinal capillary degeneration was determined after 8 months of diabetes. Flow cytometry of peripheral blood for differential expression of CCR2 in monocytes was assessed.
Results
In nondiabetic mice, CCR2 was highly expressed on monocytes, and Ccr2−/− mice lack CCR2+ monocytes in the peripheral blood. Diabetes-induced retinal superoxide, expression of proinflammatory genes Inos and Icam1, leucostasis and leucocyte-mediated cytotoxicity against retinal endothelial cells were inhibited in diabetic Ccr2-deficient mice and in chimeric mice lacking Ccr2 only from myeloid cells. In order to focus on monocytes, these cells were immuno-isolated after 2 months of diabetes, and they significantly increased monocyte-mediated endothelial cell cytotoxicity ex vivo. Monocytes from Ccr2-deficient mice caused significantly less endothelial cell death. The diabetes-induced retinal capillary degeneration was inhibited in Ccr2−/− mice and in chimeric mice lacking Ccr2 only from myeloid cells.
Conclusions/interpretation
CCR2+ inflammatory monocytes contribute to the pathogenesis of early lesions of diabetic retinopathy.
Graphical abstract
Keywords: CCR2; Diabetic retinopathy; Leucocytes; Leucostasis; Monocytes; Retinal capillary degeneration; Superoxide
