russjcardiolРоссийский кардиологический журналRussian Journal of Cardiology1560-40712618-7620«SILICEA-POLIGRAF» LLC10.15829/1560-4071-2025-6554PLSMERrussjcardiol-6554Research ArticleСТАТЬИARTICLESНаправленная доставка противовоспалительных агентов в зону ишемически-­реперфузионного повреждения миокарда с помощью наноразмерных частицTargeted anti-inflammatory agent delivery to myocardial ischemia-­reperfusion injury area using nanoparticleshttps://orcid.org/0000-0002-1896-5703ЧебуркинЮ. В.CheburkinYu. V.

Чебуркин Юрий Владимирович — к.м.н., зав. НИЛ инфекционных патогенов и биомолекулярных наноструктур.

пр. Пархоменко, д. 15, лит. Б, Санкт-­Петербург, 194156

Yuri V. Cheburkin - Cand. Sci. (Med.), Head of the Research Laboratory of Infectious Pathogens and Biomolecular Nanostructures.

Parkhomenko Ave., 15, lit. B, St. Petersburg, 194156

cheburkin_yuv@almazovcentre.ruhttps://orcid.org/0009-0006-8744-8482СмирновЕ. А.SmirnovE. A.

Смирнов Евгений Алексеевич — м.н.с., НИЛ инфекционных патогенов и биомолекулярных наноструктур; магистрант.

пр. Пархоменко, д. 15, лит. Б, Санкт-­Петербург, 194156

Evgeny A. Smirnov - Junior Researcher, Research Laboratory of Infectious Pathogens and Biomolecular Nanostructures; Master's Student.

Parkhomenko Ave., 15, lit. B, St. Petersburg, 194156

sea222777@yandex.ruhttps://orcid.org/0000-0002-8723-8622МурашкоЕ. А.MurashkoE. A.

Мурашко Екатерина Александровна — к.х.н., зав. НИЛ метаболомного и метаболического профилирования; ассистент, кафедра химии Института медицинского образования.

пр. Пархоменко, д. 15, лит. Б, Санкт-­Петербург, 194156

Ekaterina A. Murashko - Cand. Sci. (Chem.), Head of the Research Laboratory of Metabolomic and Metabolic Profiling; Assistant, Department of Chemistry, Institute of Medical Education.

Parkhomenko Ave., 15, lit. B, St. Petersburg, 194156

murashko_ea@almazovcentre.ruhttps://orcid.org/0000-0002-3666-9115КолобовА. А.KolobovA. A.

Колобов Алексей Александрович — к.б.н., в.н.с., лаборатория химии пептидов.

ул. Бехтерева, д. 1, корп. 3, литера Р, Санкт-­Петербург, 192019

Alexey A. Kolobov - Cand. Sci. (Biol.), Leading Researcher, Laboratory of Peptide Chemistry.

Bekhtereva str., 1, bld. 3, letter R, St. Petersburg, 192019

kolobov@hpb-spb.comhttps://orcid.org/0000-0003-4870-8641СитковН. О.SitkovN. O.

Ситков Никита Олегович — к.т.н., в.н.с., НИЛ инфекционных патогенов и биомолекулярных наноструктур; доцент, кафедра микро- и наноэлектроники.

пр. Пархоменко, д. 15, лит. Б, Санкт-­Петербург, 194156; Инструментальная ул., д. 2, Санкт-­Петербург

Nikita O. Sitkov - Leading Researcher, Research Laboratory of Infectious Pathogens and Biomolecular Nanostructures; Associate Professor, Department of Micro- and Nanoelectronics.

Parkhomenko Ave., 15, lit. B, St. Petersburg, 194156; Instrumentalnaya str., 2, St. Petersburg

sitkov_no@almazovcentre.ruhttps://orcid.org/0000-0001-5129-9944ГалагудзаМ. М.GalagudzaM. M.

Галагудза Михаил Михайлович — д.м.н., член-корр. РАН, директор Института экспериментальной медицины; зав. кафедрой патологической физиологии Института медицинского образования; г.н.с.

пр. Пархоменко, д. 15, лит. Б, Санкт-­Петербург, 194156; ул. Льва Толстого, д. 6-8, Санкт-­Петербург; ул. Ивана Черных, д. 31-33, лит. А, Санкт-­Петербург

Mikhail M. Gala­gudza - Dr. Sci. (Med.), Corresponding Member of the RAS, Director of the Institute of Experimental Medicine; Head of the Department of Pathological Physiology, Institute of Medical Education; Principal Researcher.

Parkhomenko Ave., 15, lit. B, St. Petersburg, 194156; Lva Tolstogo str., 6-8, St. Petersburg; Ivan Chernykh str., 31-33, lit. A, St. Petersburg

galagudza@almazovcentre.ruФГБУ Национальный медицинский исследовательский центр им. В.А. Алма­зо­ва Мин­­здрава РоссииРоссияAlmazov National Medical Research CenterRussian FederationФГУП НИИ гигиены, профпатологии и экологии человека ФМБА РоссииРоссияResearch Institute of Hygiene, Occupational Pathology and Human EcologyRussian FederationФГБУ Национальный медицинский исследовательский центр им. В.А. Алма­зо­ва Мин­­здрава России; ФГАОУ ВО Санкт-Петер­бургский государственный электротехнический университет ЛЭТИ им. В.И. Ульянова (Ленина)РоссияAlmazov National Medical Research Center; Saint Petersburg Electrotechnical University "LETI"Russian FederationФГБУ Национальный медицинский исследовательский центр им. В.А. Алма­зо­ва Мин­­здрава России; ФГБОУ ВО Первый Санкт-­­­Петер­бургский государственный медицинский университет им. акад. И.П. Павлова Минздрава России; ФГБУН Институт аналитического приборостроения РАН, Санкт-­ПетербургРоссияAlmazov National Medical Research Center; First Pavlov State Medical University; Institute for Analytical InstrumentationRussian Federation202525012026303SОбразование65546554Copyright © Чебуркин Ю.В., Смирнов Е.А., Мурашко Е.А., Колобов А.А., Ситков Н.О., Галагудза М.М., 20262026Чебуркин Ю.В., Смирнов Е.А., Мурашко Е.А., Колобов А.А., Ситков Н.О., Галагудза М.М.Cheburkin Y.V., Smirnov E.A., Murashko E.A., Kolobov A.A., Sitkov N.O., Galagudza M.M.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://russjcardiol.elpub.ru/jour/article/view/6554

Ишемически-­реперфузионное повреждение (ИРП) миокарда сопровождается асептическим воспалением, включающим процессы распознавания повреждения, геномный ответ резидентных клеток с экспрессией адгезионных молекул, цито- и хемокинов, инфильтрацию ткани лейкоцитами, а также разрешение воспаления. Противовоспалительные агенты занимают важное место в арсенале средств для лечения пациентов с ишемической болезнью сердца и профилактики сердечно-­сосудистых осложнений. Вместе с тем системное применение препаратов, подавляющих воспаление, сопряжено со значимыми побочными эффектами. Одним из путей решения имеющейся проблемы является направленная доставка молекул, подавляющих отдельные механизмы воспаления, непосредственно в зону ИРП миокарда. В обзоре рассмотрены два основных способа направленной доставки противовоспалительных активных веществ — пассивный, с помощью наночастиц, проникающих в зону ИРП благодаря повышенной проницаемости микрососудов, и активный, при котором наночастицы-­носители активного вещества модифицированы специ-фически тропными к ишемизированному миокарду направляющими лигандами. Результаты экспериментальных исследований показывают, что таргетная доставка противовоспалительных агентов сопровождается их избирательным накоплением в зоне ИРП и усилением терапевтической эффективности. Перспективы совершенствования систем направленной доставки связаны с активным таргетированием поврежденного миокарда.

Myocardial ischemia-­reperfusion injury (IRI) is accompanied by aseptic inflammation, which includes damage recognition, the genomic response of resident cells with the expression of adhesion molecules, cytokines, and chemokines, tissue leukocyte infiltration, and inflammation resolution. Anti-inflammatory agents occupy an important place in the treatment of patients with coronary artery disease (CAD) and the prevention of cardiovascular events. However, systemic use of anti-inflammatory agents is associated with significant side effects. One solution to this problem is the targeted delivery of molecules suppressing specific inflammatory mechanisms directly to the myocardial IRI area. This review describes two following methods for the targeted delivery of anti-inflammatory agents: passive delivery, using nanoparticles penetrating the IRI area due to increased microvascular permeability, and active delivery, in which the active substance-­carrying nanoparticles are modified with targeting ligands with specific tropism to the ischemic myocardium. Experimental studies demonstrate that targeted delivery of anti-inflammatory agents results in their selective accumulation in the IRI site and enhanced therapeutic efficacy. Prospects for improving targeted delivery systems are associated with active targeting of involved myocardium.

атеросклерозишемически-­реперфузионное повреждение миокардатаргетная доставкапротивовоспалительные средстванаправляющие лигандынаночастицыatherosclerosismyocardial ischemia-­reperfusion injurytargeted deliveryanti-inflammatory agentstargeting ligandsnanoparticlesРабота выполнена в рамках государственного задания ФГБУ "НМИЦ им. В.А. Алмазова" Минздрава России "Разработка метода адресной доставки на основе наноконъюгатов кардио-­таргетных пептидов" (рег. № 124021600063-1).This work was carried out within the state assignment of the Almazov National Medical Research Center "Development of a method for targeted cardiac delivery of peptides based on nanoconjugates" (registration number: 124021600063-1).ReferencesHeidenreich PA, Albert NM, Allen LA, et al. Forecasting the impact of heart failure in the United States: a policy statement from the American Heart Association. Circ Heart Fail. 2013;6(3):606-19. doi:10.1161/HHF.0b013e318291329a.Heidenreich PA, Albert NM, Allen LA, et al. Forecasting the impact of heart failure in the United States: a policy statement from the American Heart Association. Circ Heart Fail. 2013;6(3):606-19. doi:10.1161/HHF.0b013e318291329a.Шальнова С. А., Драпкина О. М., Куценко В. А. и др. Инфаркт миокарда в популяции некоторых регионов России и его прогностическое значение. Российский кардиологический журнал. 2022;27(6):4952. doi:10.15829/1560-4071-2022-4952.Shalnova SA, Drapkina OM, Kutsenko VA, et al. Myocardial infarction in the population of some Russian regions and its prognostic value. Russian Journal of Cardiology. 2022;27(6):4952. (In Russ.) doi:10.15829/1560-4071-2022-4952.Shi H, Xia Y, Cheng Y, et al. Global burden of ischaemic heart disease from 2022 to 2050: projections of incidence, prevalence, deaths, and disability-­adjusted life years. Eur Heart J Qual Care Clin Outcomes. 2025;11(4):355-66. doi:10.1093/ehjqcco/qcae049.Shi H, Xia Y, Cheng Y, et al. Global burden of ischaemic heart disease from 2022 to 2050: projections of incidence, prevalence, deaths, and disability-­adjusted life years. Eur Heart J Qual Care Clin Outcomes. 2025;11(4):355-66. doi:10.1093/ehjqcco/qcae049.Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007;357(11):1121-35. doi:10.1056/NEJMra071667.Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med. 2007;357(11):1121-35. doi:10.1056/NEJMra071667.Шляхто Е. В., Петрищев Н. Н., Галагудза М. М. и др. Кардиопротекция: фундаментальные и клинические аспекты. CПб.: НП-Принт, 2013. с. 399.Shlyakhto EV, Petrishchev NN, Galagudza MM, et al. Cardioprotection: fundamental and clinical aspects. SPb.: NP-Print, 2013. p. 399. (In Russ.)Prabhu SD, Frangogiannis NG. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. Circ Res. 2016;119(1):91-112. doi:10.1161/CIRCRESAHA.116.303577.Prabhu SD, Frangogiannis NG. The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. Circ Res. 2016;119(1):91-112. doi:10.1161/CIRCRESAHA.116.303577.Vandervelde S, van Amerongen MJ, Tio RA, et al. Increased inflammatory response and neovascularization in reperfused vs. non-reperfused murine myocardial infarction. Cardiovasc Pathol. 2006;15(2):83-90. doi:10.1016/j.carpath.2005.10.006.Vandervelde S, van Amerongen MJ, Tio RA, et al. Increased inflammatory response and neovascularization in reperfused vs. non-reperfused murine myocardial infarction. Cardiovasc Pathol. 2006;15(2):83-90. doi:10.1016/j.carpath.2005.10.006.Matter MA, Paneni F, Libby P, et al. Inflammation in acute myocardial infarction: the good, the bad and the ugly. Eur Heart J. 2024;45(2):89-103. doi:10.1093/eurheartj/ehad486.Matter MA, Paneni F, Libby P, et al. Inflammation in acute myocardial infarction: the good, the bad and the ugly. Eur Heart J. 2024;45(2):89-103. doi:10.1093/eurheartj/ehad486.Imbesi A, Greco A, Spagnolo M, et al. Targeting inflammation after acute myocardial infarction. J Am Coll Cardiol. 2025;86(15):1146-69. doi:10.1016/j.jacc.2025.07.064.Imbesi A, Greco A, Spagnolo M, et al. Targeting inflammation after acute myocardial infarction. J Am Coll Cardiol. 2025;86(15):1146-69. doi:10.1016/j.jacc.2025.07.064.Ridker PM, MacFadyen JG, Everett BM, et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secon­dary analysis from the CANTOS randomised controlled trial. Lancet. 2018;391(10118):319-28. doi:10.1016/S0140-6736(17)32814-3.Ridker PM, MacFadyen JG, Everett BM, et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secon­dary analysis from the CANTOS randomised controlled trial. Lancet. 2018;391(10118):319-28. doi:10.1016/S0140-6736(17)32814-3.Tardif JC, Kouz S, Waters DD, et al. Efficacy and Safety of Low-­Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-505. doi:10.1056/NEJMoa1912388.Tardif JC, Kouz S, Waters DD, et al. Efficacy and Safety of Low-­Dose Colchicine after Myocardial Infarction. N Engl J Med. 2019;381(26):2497-505. doi:10.1056/NEJMoa1912388.Galagudza M, Korolev D, Postnov V, et al. Passive targeting of ischemic-­reperfused myocardium with adenosine-­loaded silica nanoparticles. Int J Nanomedicine. 2012;7:1671-8. doi:10.2147/IJN.S29511.Galagudza M, Korolev D, Postnov V, et al. Passive targeting of ischemic-­reperfused myocardium with adenosine-­loaded silica nanoparticles. Int J Nanomedicine. 2012;7:1671-8. doi:10.2147/IJN.S29511.Luo Q, Sun W, Li Z, et al. Biomaterials-­mediated targeted therapeutics of myocardial ischemia-­reperfusion injury. Biomaterials. 2023;303:122368. doi:10.1016/j.biomaterials.2023.122368.Luo Q, Sun W, Li Z, et al. Biomaterials-­mediated targeted therapeutics of myocardial ischemia-­reperfusion injury. Biomaterials. 2023;303:122368. doi:10.1016/j.biomaterials.2023.122368.Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ. 2021;372:n71. doi:10.1136/bmj.n71.Page MJ, McKenzie JE, Bossuyt PM, et al. The PRISMA 2020 statement: an updated guideline for reporting systematic reviews. BMJ. 2021;372:n71. doi:10.1136/bmj.n71.Гущин И. С. Рецепторы специализированных проразрешающих медиаторов — вероятная мишень фармакологического восстановления гомеостаза при аллергическом воспалении. Иммунология. 2021;42(3):277-92. doi:10.33029/0206-4952-2021-42-3-277-292.Gushchin IS. Receptors of specialized pro-resolving mediators — a probable target of pharmacological restoration of homeostasis in allergic inflammation. Immunologiya. 2021;42(3):277-92. (In Russ.) doi:10.33029/0206-4952-2021-42-3-277-292.Zhao BH, Ruze A, Zhao L, et al. The role and mechanisms of microvascular damage in the ischemic myocardium. Cell Mol Life Sci. 2023;80(11):341. doi:10.1007/s00018-023-04998-z.Zhao BH, Ruze A, Zhao L, et al. The role and mechanisms of microvascular damage in the ischemic myocardium. Cell Mol Life Sci. 2023;80(11):341. doi:10.1007/s00018-023-04998-z.Leuschner F, Dutta P, Gorbatov R, et al. Therapeutic siRNA silencing in inflammatory monocytes in mice. Nat Biotechnol. 2011;29(11):1005-10. doi:10.1038/nbt.1989.Leuschner F, Dutta P, Gorbatov R, et al. Therapeutic siRNA silencing in inflammatory monocytes in mice. Nat Biotechnol. 2011;29(11):1005-10. doi:10.1038/nbt.1989.Nagaoka K, Matoba T, Mao Y, et al. A New Therapeutic Modality for Acute Myocardial Infarction: Nanoparticle-­Mediated Delivery of Pitavastatin Induces Cardioprotection from Ischemia-­Reperfusion Injury via Activation of PI3K/Akt Pathway and Anti-­Inflammation in a Rat Model. PLoS One. 2015;10(7):e0132451. doi:10.1371/journal.pone.0132451.Nagaoka K, Matoba T, Mao Y, et al. A New Therapeutic Modality for Acute Myocardial Infarction: Nanoparticle-­Mediated Delivery of Pitavastatin Induces Cardioprotection from Ischemia-­Reperfusion Injury via Activation of PI3K/Akt Pathway and Anti-­Inflammation in a Rat Model. PLoS One. 2015;10(7):e0132451. doi:10.1371/journal.pone.0132451.Margulis K, Neofytou EA, Beygui RE, Zare RN. Celecoxib Nanoparticles for Therapeutic Angiogenesis. ACS Nano. 2015;9(9):9416-26. doi:10.1021/acsnano.5b04137.Margulis K, Neofytou EA, Beygui RE, Zare RN. Celecoxib Nanoparticles for Therapeutic Angiogenesis. ACS Nano. 2015;9(9):9416-26. doi:10.1021/acsnano.5b04137.Somasuntharam I, Yehl K, Carroll SL, et al. Knockdown of TNF-α by DNAzyme gold nanoparticles as an anti-inflammatory therapy for myocardial infarction. Biomaterials. 2016;83:12-22. doi:10.1016/j.biomaterials.2015.12.022.Somasuntharam I, Yehl K, Carroll SL, et al. Knockdown of TNF-α by DNAzyme gold nanoparticles as an anti-inflammatory therapy for myocardial infarction. Biomaterials. 2016;83:12-22. doi:10.1016/j.biomaterials.2015.12.022.Cuadrado I, Piedras MJ, Herruzo I, et al. EMMPRIN-Targeted Magnetic Nanoparticles for In Vivo Visualization and Regression of Acute Myocardial Infarction. Theranostics. 2016;6(4):545-57. doi:10.7150/thno.13352.Cuadrado I, Piedras MJ, Herruzo I, et al. EMMPRIN-Targeted Magnetic Nanoparticles for In Vivo Visualization and Regression of Acute Myocardial Infarction. Theranostics. 2016;6(4):545-57. doi:10.7150/thno.13352.Nakano Y, Matoba T, Tokutome M, et al. Nanoparticle-­Mediated Delivery of Irbesartan Induces Cardioprotection from Myocardial Ischemia-­Reperfusion Injury by Antagonizing Monocyte-­Mediated Inflammation. Sci Rep. 2016;6:29601. doi:10.1038/srep29601.Nakano Y, Matoba T, Tokutome M, et al. Nanoparticle-­Mediated Delivery of Irbesartan Induces Cardioprotection from Myocardial Ischemia-­Reperfusion Injury by Antagonizing Monocyte-­Mediated Inflammation. Sci Rep. 2016;6:29601. doi:10.1038/srep29601.Maranhão RC, Guido MC, de Lima AD, et al. Methotrexate carried in lipid core nanoparticles reduces myocardial infarction size and improves cardiac function in rats. Int J Nanomedicine. 2017;12:3767-84. doi:10.2147/IJN.S129324.Maranhão RC, Guido MC, de Lima AD, et al. Methotrexate carried in lipid core nanoparticles reduces myocardial infarction size and improves cardiac function in rats. Int J Nanomedicine. 2017;12:3767-84. doi:10.2147/IJN.S129324.Fujiwara M, Matoba T, Koga JI, et al. Nanoparticle incorporating Toll-like receptor 4 inhibitor attenuates myocardial ischaemia-­reperfusion injury by inhibiting monocyte-­mediated inflammation in mice. Cardiovasc Res. 2019;115(7):1244-55. doi:10.1093/cvr/cvz066.Fujiwara M, Matoba T, Koga JI, et al. Nanoparticle incorporating Toll-like receptor 4 inhibitor attenuates myocardial ischaemia-­reperfusion injury by inhibiting monocyte-­mediated inflammation in mice. Cardiovasc Res. 2019;115(7):1244-55. doi:10.1093/cvr/cvz066.Tokutome M, Matoba T, Nakano Y, et al. Peroxisome proliferator-­activated receptor-­gamma targeting nanomedicine promotes cardiac healing after acute myocardial infarction by skewing monocyte/macrophage polarization in preclinical animal models. Cardiovasc Res. 2019;115(2):419-31. doi:10.1093/cvr/cvy200.Tokutome M, Matoba T, Nakano Y, et al. Peroxisome proliferator-­activated receptor-­gamma targeting nanomedicine promotes cardiac healing after acute myocardial infarction by skewing monocyte/macrophage polarization in preclinical animal models. Cardiovasc Res. 2019;115(2):419-31. doi:10.1093/cvr/cvy200.Yajima S, Miyagawa S, Fukushima S, et al. Prostacyclin Analogue-­Loaded Nanoparticles Attenuate Myocardial Ischemia/Reperfusion Injury in Rats. JACC Basic Transl Sci. 2019;4(3):318-31. doi:10.1016/j.jacbts.2018.12.006.Yajima S, Miyagawa S, Fukushima S, et al. Prostacyclin Analogue-­Loaded Nanoparticles Attenuate Myocardial Ischemia/Reperfusion Injury in Rats. JACC Basic Transl Sci. 2019;4(3):318-31. doi:10.1016/j.jacbts.2018.12.006.Richart AL, Reddy M, Khalaji M, et al. Apo AI Nanoparticles Delivered Post Myocardial Infarc­tion Moderate Inflammation. Circ Res. 2020;127(11):1422-36. doi:10.1161/CIRCRESAHA.120.316848.Richart AL, Reddy M, Khalaji M, et al. Apo AI Nanoparticles Delivered Post Myocardial Infarc­tion Moderate Inflammation. Circ Res. 2020;127(11):1422-36. doi:10.1161/CIRCRESAHA.120.316848.Ikeda G, Matoba T, Ishikita A, et al. Nanoparticle-­Mediated Simultaneous Targeting of Mitochondrial Injury and Inflammation Attenuates Myocardial Ischemia-­Reperfusion Injury. J Am Heart Assoc. 2021;10(12):e019521. doi:10.1161/JAHA.120.019521.Ikeda G, Matoba T, Ishikita A, et al. Nanoparticle-­Mediated Simultaneous Targeting of Mitochondrial Injury and Inflammation Attenuates Myocardial Ischemia-­Reperfusion Injury. J Am Heart Assoc. 2021;10(12):e019521. doi:10.1161/JAHA.120.019521.Wang L, Peng Y, Song L, et al. Colchicine-­Containing Nanoparticles Attenuates Acute Myocardial Infarction Injury by Inhibiting Inflammation. Cardiovasc Drugs Ther. 2022;36(6):1075-89. doi:10.1007/s10557-021-07239-2.Wang L, Peng Y, Song L, et al. Colchicine-­Containing Nanoparticles Attenuates Acute Myocardial Infarction Injury by Inhibiting Inflammation. Cardiovasc Drugs Ther. 2022;36(6):1075-89. doi:10.1007/s10557-021-07239-2.Wang T, Wang Y, Zhang Y, et al. Drug-­Loaded Mesoporous Polydopamine Nanoparticles in Chitosan Hydrogels Enable Myocardial Infarction Repair through ROS Scavenging and Inhibition of Apoptosis. ACS Appl Mater Interfaces. 2024;16(45):61551-64. doi:10.1021/acsami.4c08155.Wang T, Wang Y, Zhang Y, et al. Drug-­Loaded Mesoporous Polydopamine Nanoparticles in Chitosan Hydrogels Enable Myocardial Infarction Repair through ROS Scavenging and Inhibition of Apoptosis. ACS Appl Mater Interfaces. 2024;16(45):61551-64. doi:10.1021/acsami.4c08155.Карпов А. А., Ивкин Д. Ю., Драчева А. В. и др. Моделирование постинфарктной сердечной недостаточности путем окклюзии левой коронарной артерии у крыс: техника и методы морфофункциональной оценки Биомедицина. 2014;3:32-48.Karpov AA, Ivkin DYu, Dracheva AV, et al. Rat model of post-infarct heart failure by left coronary artery occlusion: technical aspects, functional and morphological assessment. Biomedicine. 2014;3:32-48. (In Russ.)Wang J, Seo MJ, Deci MB, et al. Effect of CCR2 inhibitor-­loaded lipid micelles on inflammatory cell migration and cardiac function after myocardial infarction. Int J Nanomedicine. 2018;13:6441-51. doi:10.2147/IJN.S178650.Wang J, Seo MJ, Deci MB, et al. Effect of CCR2 inhibitor-­loaded lipid micelles on inflammatory cell migration and cardiac function after myocardial infarction. Int J Nanomedicine. 2018;13:6441-51. doi:10.2147/IJN.S178650.Tartuce LP, Pacheco Brandt F, Dos Santos Pedroso G, et al. 2-methoxy-­isobutyl-isonitrile-­conjugated gold nanoparticles improves redox and inflammatory profile in infarcted rats. Colloids Surf B Biointerfaces. 2020;192:111012. doi:10.1016/j.colsurfb.2020.111012.Tartuce LP, Pacheco Brandt F, Dos Santos Pedroso G, et al. 2-methoxy-­isobutyl-isonitrile-­conjugated gold nanoparticles improves redox and inflammatory profile in infarcted rats. Colloids Surf B Biointerfaces. 2020;192:111012. doi:10.1016/j.colsurfb.2020.111012.Wei Y, Zhu M, Li S, et al. Engineered Biomimetic Nanoplatform Protects the Myocardium Against Ischemia/Reperfusion Injury by Inhibiting Pyroptosis. ACS Appl Mater Interfaces. 2021;13(29):33756-66. doi:10.1021/acsami.1c03421.Wei Y, Zhu M, Li S, et al. Engineered Biomimetic Nanoplatform Protects the Myocardium Against Ischemia/Reperfusion Injury by Inhibiting Pyroptosis. ACS Appl Mater Interfaces. 2021;13(29):33756-66. doi:10.1021/acsami.1c03421.Huang C, Zhou S, Chen C, et al. Biodegradable Redox-­Responsive AIEgen-­Based-­Covalent Organic Framework Nanocarriers for Long-­Term Treatment of Myocardial Ischemia/Reperfusion Injury. Small. 2022;18(47):e2205062. doi:10.1002/smll.202205062.Huang C, Zhou S, Chen C, et al. Biodegradable Redox-­Responsive AIEgen-­Based-­Covalent Organic Framework Nanocarriers for Long-­Term Treatment of Myocardial Ischemia/Reperfusion Injury. Small. 2022;18(47):e2205062. doi:10.1002/smll.202205062.Lan M, Hou M, Yan J, et al. Cardiomyocyte-­targeted anti-inflammatory nanotherapeutics against myocardial ischemia reperfusion (IR) injury. Nano Res. 2022;15(10):9125-34. doi:10.1007/s12274-022-4553-6.Lan M, Hou M, Yan J, et al. Cardiomyocyte-­targeted anti-inflammatory nanotherapeutics against myocardial ischemia reperfusion (IR) injury. Nano Res. 2022;15(10):9125-34. doi:10.1007/s12274-022-4553-6.Hou M, Wu X, Zhao Z, et al. Endothelial cell-targeting, ROS-ultrasensitive drug/siRNA co-delivery nanocomplexes mitigate early-­stage neutrophil recruitment for the anti-inflammatory treatment of myocardial ischemia reperfusion injury. Acta Biomater. 2022;143:344-55. doi:10.1016/j.actbio.2022.02.018.Hou M, Wu X, Zhao Z, et al. Endothelial cell-targeting, ROS-ultrasensitive drug/siRNA co-delivery nanocomplexes mitigate early-­stage neutrophil recruitment for the anti-inflammatory treatment of myocardial ischemia reperfusion injury. Acta Biomater. 2022;143:344-55. doi:10.1016/j.actbio.2022.02.018.Weng X, Tan H, Huang Z, et al. Targeted delivery and ROS-responsive release of Resolvin D1 by platelet chimeric liposome ameliorates myocardial ischemia-­reperfusion injury. J Nanobiotechnology. 2022;20(1):454. doi:10.1186/s12951-022-01652-x.Weng X, Tan H, Huang Z, et al. Targeted delivery and ROS-responsive release of Resolvin D1 by platelet chimeric liposome ameliorates myocardial ischemia-­reperfusion injury. J Nanobiotechnology. 2022;20(1):454. doi:10.1186/s12951-022-01652-x.Tan Y, Wang X, Gu Y, et al. Neutrophil and endothelial cell membranes coassembled roflumilast nanoparticles attenuate myocardial ischemia/reperfusion injury. Nanomedicine. 2024;19(9):779-97. doi:10.2217/nnm-2023-0313.Tan Y, Wang X, Gu Y, et al. Neutrophil and endothelial cell membranes coassembled roflumilast nanoparticles attenuate myocardial ischemia/reperfusion injury. Nanomedicine. 2024;19(9):779-97. doi:10.2217/nnm-2023-0313.

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