clinmedКлиническая медицинаClinical Medicine (Russian Journal)0023-21492412-1339ООО «Медицинское информационное агентство»10.30629/0023-2149-2021-99-11-12-608-614clinmed-316Research ArticleОБЗОРЫ И ЛЕКЦИИREVIEWS AND LECTURESНетоз как фактор, способствующий развитию и прогрессированию сахарного диабета и его микрососудистых осложненийNeutrophil extracellular traps (NETosis) as a factor contributing to the development and progression of diabetes mellitus and its microvascular complicationshttps://orcid.org/0000-0003-4973-039XАйтбаевК. А.AitbaevK. A.

Айтбаев Кубаныч Авенович  — д-р мед. наук, профессор, руководитель лаборатории патологической физиологии, член правления Общества специалистов по хронической болезни почек Кыргызстана

720040, Бишкек

Aitbaev Kubanych A.

720040, Bishkek

https://orcid.org/0000-0001-8513-9279МуркамиловИ. Т.MurkamilovI. T.

Муркамилов Илхом Торобекович — канд. мед. наук, исполняющий обязанности доцента кафедры факультетской терапии; старший преподаватель, нефролог, председатель правления Общества специалистов по хронической болезни почек Кыргызстана

720020, Бишкек; 720000, Бишкек

Murkamilov Ilkhom T.

720020, Bishkek; , 720000, Bishkek

murkamilov.i@mail.ruhttps://orcid.org/0000-0002-2682-4417ФоминВ. В.FominV. V.

Фомин Виктор Викторович — д-р мед. наук, профессор, член-корр. РАН, зав. кафедрой факультетской терапии №1 Института клинической медицины им. Н.В. Склифосовского, проректор по клинической работе и дополнительному профессиональному образованию

119991, Москва

Fomin Viktor V.

119991, Moscow

https://orcid.org/0000-0003-3007-8127КудайбергеноваИ. О.KudaibergenovaI. O.

Кудайбергенова Индира Орозобаевна  — д-р мед. наук, профессор, ректор

720020, Бишкек

Kudaibergenova Indira O.

720020, Bishkek

https://orcid.org/0000-0003-0632-6653ЮсуповФ. А.YusupovF. A.

Юсупов Фуркат Абдулахатович — д-р мед. наук, профессор, зав. кафедрой неврологии, нейрохирургии и психиатрии медицинского факультета Ошского государственного университета, член правления Общества специалистов по хронической болезни почек Кыргызстана, главный невролог Южного региона Кыргызстана

723500, Ош

Yusupov Furkat A.

723500, Osh

Научно-исследовательский институт молекулярной биологии и медициныКыргызстанScientifi c and Research Institute of Molecular Biology and MedicineKyrgyzstanКыргызская государственная медицинская академия имени И.К. Ахунбаева; ГОУ ВПО «Кыргызско-Российский славянский университет»КыргызстанKyrgyz State Medical Academy named after Akhunbaev I.K.; Kyrgyz-Russian Slavic UniversityKyrgyzstanФГАОУ ВО «Первый Московский государственный медицинский университет имени И.М. Сеченова» Минздрава России (Сеченовский Университет)РоссияFirst Moscow State Medical University of the Ministry of Healthcare of the Russian Federation (Sechenov University)Russian FederationКыргызская государственная медицинская академия имени И.К. АхунбаеваКыргызстанKyrgyz State Medical Academy named after Akhunbaev I.K.KyrgyzstanОшский государственный университетКыргызстанOsh State UniversityKyrgyzstan2021040320229911-12608614Copyright © Айтбаев К.А., Муркамилов И.Т., Фомин В.В., Кудайбергенова И.О., Юсупов Ф.А., 20222022Айтбаев К.А., Муркамилов И.Т., Фомин В.В., Кудайбергенова И.О., Юсупов Ф.А.Aitbaev K.A., Murkamilov I.T., Fomin V.V., Kudaibergenova I.O., Yusupov F.A.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.clinmedjournal.com/jour/article/view/316

Нетоз — новая форма гибели клеток — привлекает в последние годы пристальное внимание исследователей из-за его двойственного влияния на патологический процесс. Будучи изначально защитной реакцией врожденной иммунной защиты, направленной на улавливание и обезвреживание проникших в организм патогенов (бактерий, вирусов и грибов), нетоз при его чрезмерной активации может, напротив, способствовать прогрессированию заболевания, вызывая аутоиммунизацию, повреждение окружающей ткани или возникновение атеротромботических событий. В этом обзоре представлены данные о том, что образование в процессе нетоза внеклеточных ловушек нейтрофилов, называемых NETs, играет важную роль в патогенезе сахарного диабета (СД) и его микрососудистых осложнений. Например, при СД 1-го типа смерть β-клеток способствует секвестрации нейтрофилов в поджелудочную железу и четко коррелирует с увеличением нетоза. У пациентов с СД 2-го типа продукты высвобождения NETs также значительно повышены. Повышенный уровень дцДНК, маркера нетоза, коррелирует с развитием сердечно-сосудистых заболеваний и диабетической болезнью почек, что также согласуется со способствующей ролью нетоза в патогенезе таких диабетических осложнений, как нарушение заживления ран и диабетическая ретинопатия. Механизмы, связывающие нетоз с высоким уровнем глюкозы, не совсем понятны, поскольку нетоз повышен и у пациентов с диабетом, которые строго контролируют уровень глюкозы. Можно лишь предполагать, что нетоз не является следствием нарушения гликемического контроля, а, напротив, вызывает гипергликемию, которая в еще большей степени повышает исходно высокий уровень нетоза у пациентов с диабетом.

NETosis, a new form of cell death, has attracted close attention of researchers in recent years due to its dual eff ect on the pathological process. Being initially a defense reaction of the innate immune defenсe aimed at trapping and neutralizing pathogens (bacteria, viruses and fungi) that have invaded the body, NETosis, in case of excessive activation, has an opposite eff ect. It can contribute to the progression of the disease, causing autoimmunization, damage to surrounding tissue, or the occurrence of atherothrombotic events. This review presents data dealing with the formation of extracellular traps of neutrophils, called NETs. NETosis plays an important role in the pathogenesis of diabetes mellitus (DM) and its microvascular complications. For example, in type 1 DM, β-cell death promotes sequestration of neutrophils into the pancreas and is clearly correlated with increased NETosis. In patients with type 2 DM, the release is also signifi cantly increased. High levels of dsDNA, a marker of NETosis, are correlated with the development of cardiovascular disease and DM caused kidney disease, which is also consistent with the contributing role of NETosis in the pathogenesis of diabetic complications such as impaired wound healing and diabetic retinitis. The mechanisms linking NETosis with high glucose levels are not clearly understood, as NETosis is also increased in diabetic patients strictly controlling glucose levels. One can only assume that NETosis is not a consequence of impaired glycemic control. On the contrary, it causes hyperglycemia, which further increases the initially high level of NETosis in patients with DM.

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The authors declare that there are no conflicts of interest present.